What percentage of DNA is found in eukaryotic mitochondria. Mother's mitochondrial DNA

A significant part of the readers of my blogs, of course, to one degree or another have an idea of the essence and nature of inheritance of mitochondrial DNA. Thanks to the availability of commercial testing, many of my (over)readers have identified mitochondrial haplotypes in individual regions of the mitochondrion (CR, HVS1, HVS2), and some even have a complete mitochondrial sequence (all 16571 positions). Thus, many were able to shed light on their “deep genealogy”, going back to the common point of coalition of all currently existing female genetic lines. Romantic popgeneticists called this point “mitochondrial Eve,” although this point is still just a mathematical abstraction and, because of this, any name is purely conventional.

A short excursion for beginners.
Mitochondrial DNA (hereinafter mtDNA) is passed from mother to child. Since only women can pass mtDNA to their offspring, mtDNA testing provides information about the mother, her mother, and so on through the direct maternal line. Both men and women receive mtDNA from their mother, which is why both men and women can participate in mtDNA testing. Although mutations do occur in mtDNA, their frequency is relatively low. Over thousands of years, these mutations have accumulated, and for this reason, the female line in one family is genetically different from another. After humanity spread across the planet, mutations continued to randomly appear in populations separated by distance from the once united human race. For this reason, mtDNA can be used to determine the geographic origin of a given family group. The results of mtDNA testing are compared with the so-called “Cambridge Standard Sequence” (CRS) - the first mtDNA sequence established in 1981 in Cambridge (* note - the use of CRS as a reference mitosequence is currently under review). As a result, scientists establish the haplotype of the person being studied. A haplotype is your individual genetic characteristic. When you look at it, mtDNA is your set of deviations from the “Cambridge standard sequence”. After comparing your sequence with sequences from the database, your haplogroup is determined. A haplogroup is a genetic characteristic of a certain community of people who had one common “great-grandmother”, more recent than “mitochondrial Eve”. Their ancient ancestors often moved in the same group during migrations. The haplogroup shows which genealogical branch of humanity you belong to. They are designated by letters of the alphabet, from A to Z, plus numerous subgroups. For example, European haplogroups - H, J, K, T, U, V, X. Middle Eastern - N and M. Asian - A, B, C, D, F, G, M, Y, Z. African - L1, L2 , L3 and M1. Polynesian - B. American Indians - A, B, C, D, and rarely X. Recently, N1, U4, U5 and W have been added to the European haplogroups.

Let's focus on European mitohaplogroups - H, J, K, T, U, V, X, N1, U4, U5 and W. Most of them, in turn, split into daughter subclades (daughter branches, for example, the daughter subclade of haplogroup U5 - subclade U5b1 (“Ursula”), whose distribution peak occurs in the Baltic states and Finland. It is worth noting that matriarchs of female lines are often simply called by female names. The foundation of this tradition was laid by the author of the book “Seven Daughters of Eve” Brian Sykes, who came up with names for the supposed ancestors of most of the European population - Ursula (haplogroup U), Ksenia (X), Elena (H), Velda (V), Tara (T), Catherine (K) and Jasmine (J). You can trace and map the main roads along which they and the rest of our great-great-grandmothers roamed in time and space, and calculate the estimated time for each fork - the appearance of a new mutation, from the first “daughters of Eve” to the most recent - haplogroups I and V, which "only" about 15,000 years.

I often ask the question: how is nuclear DNA different from mtDNA? According to modern scientific concepts, billions of years ago mitochondria were independent bacteria that settled in the cells of primitive eukaryotic (having a cell nucleus with linear chromosomes) organisms and “took over” the function of producing heat and energy in the host cells. During their life together, they lost some of their genes as unnecessary while living with everything ready, some were transferred to nuclear chromosomes, and now the double ring of human mtDNA consists of only 16,569 nucleotide base pairs. The majority of the mitochondrial genome is occupied by 37 genes. Due to the high concentration of oxygen free radicals (by-products of glucose oxidation) and the weakness of the mechanism for repairing errors during DNA copying, mutations in mtDNA occur an order of magnitude more often than in nuclear chromosomes. The replacement, loss or addition of one nucleotide here occurs approximately once every 100 generations - about 2500 years. Mutations in mitochondrial genes - disruptions in the functioning of cellular energy plants - very often cause hereditary diseases. The only function of mitochondria is the oxidation of glucose to carbon dioxide and water and synthesis using the energy of cellular fuel released during this process - ATP and the universal reducing agent (proton carrier) NADH. (NADH is nicotinamide adenine dinucleotide - try to pronounce it without hesitation.) Even this simple task requires dozens of enzymes, but most of the protein genes necessary for the work and maintenance of mitochondria have long been transferred to the chromosomes of the “host” cells. In mtDNA, only the transfer RNA genes that supply amino acids to the ribosomes synthesizing proteins remain (indicated by single-letter Latin symbols of the corresponding amino acids), two ribosomal RNA genes - 12s RNA and 16s RNA (the genes for mitochondrial ribosome proteins are located in the cell nucleus) and some (not all) genes proteins of the main mitochondrial enzymes - NADH dehydrogenase complex (ND1-ND6, ND4L), cytochrome c oxidase (COI-III), cytochrome b (CYTb) and two protein subunits of the ATP synthetase enzyme (ATPase8 and 6). For the needs of molecular or DNA genealogy, a non-coding region is used - D-loop, consisting of two hypervariable regions, low and high resolution - HVR1 (GVS1) and HVR2 (GVS2).

It is worth saying a few words about the importance of studying mtDNA from the point of view of medical genetics.
Of course, studies have already been carried out on the association of certain diseases with individual female genetic lines. For example, one study suggested that the decomposition of oxidative phosphorylation of mitochlorions associated with the SNP defining the J(asmine) haplogroup causes increased body temperature in the phenotype of carriers of this haplogroup. This is associated with the increased presence of this haplogroup in northern Europe, in particular in Norway. In addition, people with mitochondrial haplogroup J, according to another study, develop AIDS faster and die faster compared to other HIV-infected people. The studies indicated that phylogenetically significant mitochondrial mutations entailed the pattern of gene expression in the phenotype.

Further, J's sister mitochondrial haplogroup T is associated with reduced sperm motility in men. According to a publication by the Department of Biochemistry and Molecular Cellular Biology of the University of Zaragoza, haplogroup T represents a weak genetic predisposition to asthenozoospermia. According to some studies, the presence of haplogroup T is associated with an increased risk of coronary artery disease. According to another study, T carriers are less likely to develop diabetes. Several pilot medical studies have shown that having haplogroup T is associated with a reduced risk of Parkinson's and Alzheimer's diseases.

However, the very next example shows that the results of analyzing the connection between female genetic lines and diseases often contradict each other. For example, carriers of the oldest European mitohaplogroup UK are little susceptible to acquired immune deficiency syndrome. And at the same time, one subgroup, U5a, is considered particularly susceptible to acquired immune deficiency syndrome.

Earlier studies have shown a positive correlation between membership in haplogroup U and the risk of prostate and colorectal cancer. Haplogroup K (Catherine), descending from the UK through the U8 subclade, as well as its parental lines, is characterized by an increased risk of stroke and chronic progressive ophthalmoplegia.

Men belonging to the dominant female line H in Europe (Helen - Helena, a branch of the combined group H) are characterized by the lowest risk of asthenozoospermia (a disease in which sperm motility decreases). This haplogroup is also characterized by high body resistance and resistance to the progression of AIDS. At the same time, , H is characterized by a high risk of developing Alzheimer's disease. By comparison, the risk of developing Parkinson's disease in carriers of the female genetic line H (Helen) is much higher than the similar risk in representatives of the line (JT). In addition, representatives of Lynn H have the highest resistance to sepsis.

Representatives of the mitochondrial lines I, J1c, J2, K1a, U4, U5a1 and T have a reduced (compared to the average) risk of developing Parkinson's disease. Women of the genetic lines I (Irene), J (Jasmine) and T (Tara) gave birth to more of all centenarians, which is why popgeneticists jokingly call these mitohaplogroups haplogroups of centenarians. But not everything is so good. Some members of the subclades of haplogroups J and T (especially J2) suffer from a rare genetically determined disease (Leber hereditary optic neuropathy), associated with the expression of a gene responsible for maternally inherited blindness.

Belonging to mitohaplogroup N is a factor in the development of breast cancer. However, the same applies to other European mitohaplogroups (H, T, U, V, W, X), with the exception of K. Finally, carriers of the female mitochondrial line X (“Ksenia”) have a mutation in the mitochondria that increases the risk of developing diabetes II type, cardiomyopathy and endometrial cancer. Representatives of the combined macromitohaplogroup IWX have the highest resistance to the development of AIDS.

Mitochondria also play an important role in sports genetics, which has emerged relatively recently.

Often, while reading descriptions of sports drugs and food supplements, I came across a mention that one or another active element of the drug accelerates the metabolism or transport of certain compounds into the mitochondria. This primarily concerns L-carnitine, creatine and BCAA. Since the mitochondrion acts as an energy generator in the cell, these observations seem logical and plausible to me.

Therefore, let us consider this issue in some more detail.

According to some scientists, energy deficiency leads to early aging of the body. The less energy there is in the cells, the less effort will be directed towards restoration and removal of toxins. As they say, “I don’t care about fat, I wish I was alive.” But there is always a way out:a healthy diet plus little biochemical tweaks can restart cellular power plants. And the first thing they advise you to remember is carnitine.

Beginning in adulthood, mitochondria, cellular power plants, begin to slow down, which leads to a decrease in energy production. The cell is moving towards austerity, in which the “afterburner” mode is not worth even dreaming of. Lack of energy leads to dysfunction of other cellular organelles and again affects mitochondria. Vicious circle. This is aging, or more precisely, its internal manifestation.

“You are only as young as your mitochondria,” nutritionist Robert Crichon likes to say. Having devoted many years to studying the biochemistry of cells, he found one way to influence the energy production of mitochondria, that is, aging. This method is carnitine and its active form L-carnitine.

Carnitine is not an amino acid because it does not contain an amino group (NH2). It is more like a coenzyme or, if you prefer, a water-soluble vitamin-like compound. Why does carnitine attract the attention of nutritionists?

As you know, fatty acids are the main fuel for muscles, especially the myocardium. About 70% of energy is produced in muscles from burning fat. Carnitine transports long-chain fatty acids across the mitochondrial membrane. A small amount of carnitine (about 25%) is synthesized by the body from the amino acid lysine. We must get the remaining 75% from food.

But today we get too little carnitine. It is said that our ancestors consumed at least 500 mg of carnitine daily. The average person in modern society receives only 30-50 mg per day from food...

Carnitine deficiency leads to decreased energy production and degeneration. Less energy means poorer physiological reserves. The classic picture is of elderly people whose bodies are experiencing an “energy crisis.” If the body had enough energy, it could successfully build and renew cell membranes, maintain the integrity of cellular structures, and protect genetic information. Our immune system also depends on adequate energy production.

Robert Crichon believes that we need more carnitine as the body begins to decline. This is a step towards rejuvenating and energizing cells so that they can function better and also protect themselves from free radicals and pathogens. [ By the way, a year and a half ago I conducted a pilot examination with a physiologist to determine biological age. According to the physiologist’s table, the measurement results most accurately corresponded to the biological age of 28 years. If Mr. Robert Crichon is right, then my mitochondria are 7 years younger than my passport age)). But many of my peers are already living in debt from nature (again, at the expense of their mitochondria)].

Meat, fish, milk, eggs, cheese and other animal products generally contain enough carnitine. Mutton and lamb are particularly potent sources. Avocado and tempeh are the most preferred plant sources.

Of course, animals used to graze on pastures and eat grass. This was great because in this case, animal products contained large amounts of carnitine and healthy omega-3 fatty acids, which complement each other. This allowed our ancestors' bodies to effectively burn fat and have a strong body. Now cattle are fed grain, which is dominated by omega-6 fatty acids, which have a pro-inflammatory effect, and carnitine levels have decreased. That's why now, eating red meat every day is no longer a healthy alternative. But let's stop there.

There is one more point that is worth mentioning. It would be naive to claim that carnitine can save a person from aging once and for all. No, it would be too easy for humanity, although many might want to believe it.

Carnitine, like other beneficial substances that activate metabolism, is just one of many helpers. However, it is not able to radically stop the cellular clock, although it is probably able to slow it down.

It was found that the work of the ischemic myocardium stops when the cellular resources of creatine phosphoric acid are exhausted, although approx. 90% adenosine triphosphate. This demonstrated that adenosine triphosphate is distributed unevenly throughout the cell. Not all of the adenosine triphosphate found in the muscle cell is used, but only a certain part of it, concentrated in the myofibrils. The results of further experiments demonstrated that the connection between cellular stores of adenosine triphosphate is carried out by creatine phosphoric acid and creatine kinase isoenzymes. Under normal conditions, the adenosine triphosphate molecule synthesized in the mitochondria transfers energy to creatine, which, under the influence of the isoenzyme creatine kinase, is converted into creatine phosphoric acid. Creatine phosphoric acid moves to the localization of creatine kinase reactions, where other creatine kinase isoenzymes ensure the regeneration of adenosine triphosphate from creatine phosphoric acid and adenosine diphosphate. The creatine released in this case moves into the mitochondria, and adenosine triphosphate is used to produce energy, incl. for muscle tension. The intensity of energy circulation in the cell along the creatine phosphorus pathway is much greater than the rate of penetration of adenosine triphosphate into the cytoplasm. This is the reason for the drop in the concentration of creatine phosphoric acid in the cell, and causes depression of muscle tension even when the main cellular supply of adenosine triphosphate is unaffected.

Unfortunately, people involved in sports genetics pay very little attention to mitochondria. I have not yet seen a study of the results of bodybuilders divided into control groups based on belonging to mitochondrial groups (assuming that their other “indicators” are the same). For example, the experimental design could look like this: we select bodybuilders of the same age, weight, height, muscle composition and experience. We invite them to perform a set of identical strength exercises (for example, the maximum number of sets of bench press with a weight of 95-100 kg.) We compare the results and analyze them based on a priori information about the mitogroups of athletes. Then we give the athletes a combo diet of creatine, levocarnitine, glutamine and amino acids. After some time, we repeat the test and compare the results and draw conclusions about the presence/absence of a correlation with the mtDNA type.

I think that my amateur research on mitochondria can ultimately enlighten humanity. True, I am interested in mitochondria not only and not so much in genealogy and medical issues, but in issues of psychogenetics, in particular aspects of interaction between people of different mitohapogroups. I took the liberty of calling this area of research psychosocionics. Taking advantage of the rare opportunity to observe (for 4 years) the interaction of people of different mitohaplogroups on at least 5 English-language forums and 2 Russian-language forums, I noticed an interesting trend. Unfortunately, I did not have time to clearly articulate this pattern in the discursive terms of the scientific language of popgenetics; everything is still at the level of preliminary remarks. But perhaps, if I can formulate my observation, it will go down in the history of population genetics as Verenich-Zaporozhchenko law.

My observations are based on the study of interactions between the three main European summary mitohaplogroups (JT, HV, UK). Unfortunately, European mitohaplogroups I, W, X (as well as exotic and minor mitogroups) due to the non-representativeness of the sample were not included in the field of my research. Briefly, these observations boil down to the following points:

1) the most dense and productive interaction is observed between representatives of one combined haplogroup (for example, between representatives of different subclades J and T). Perhaps this fact can be explained by an evolutionary mechanism that determines at the genetic level (let me remind you that mitoDNA is inherited strictly through the maternal line) the attachment of a child to his mother at an early age. Clark-Stewart, in her study of tripartite relationships in many families, discovered that the influence of the mother on the child is direct character, while the father often influences the baby indirectly - through the mother (Clarke-Stewart K.A., 1978). This influence is subsequently interpolated on interaction with representatives of similar mitohaplogroups (the psychogenetic basis of this influence has not yet been scientifically identified). Therefore, it is not surprising that among their fellow haplogroups people find the most reliable like-minded people

2) representatives of JT and HV are antipodes in relation to each other - it is between them that the most antagonistic interaction is observed, often leading to conflicts. The reasons for the antagonism remain to be studied

3) representatives of the UK mitogroup, as a rule, are characterized by a neutral attitude towards both JT and HV. Relations with both groups are purely business-like, neutral-friendly.

Since I was interested in the reasons for such an obvious division, I turned for advice to Valery Zaporozhchenko, the world's leading specialist in mtDNA (he is the author of one of the most effective phylogenetic programs MURKA, has the world's largest private collection of mitohaplotypes and complete genomic sequences, and is co-author of several major publications on mitoDNA).Valery gave a somewhat unusual, but if you think about it, logical answer.The gist of his answer was that the antagonism between JT and HV could be explained by “genetic memory.” The fact is that haplogroup HV penetrated into Europe somewhere at the turn of the Mesolithic and Neolithic through the northern route.In parallel with this haplogroup, the female genus JT entered Europe, but the migration route ran somewhat to the south. Most likely, there was some competition between both groups (JT and HV), since both JT and HV occupied the same niche (Neolithic farmers). TOBy the way, the same historical introspection explains the neutrality of the UK mitogroup in relation to HV and JT. As is generally accepted now, UK (being the oldest mitogroup of Europe) at the dawn of the Neolithic revolution and the appearance of the above-mentioned NeolithicThese groups were represented mainly among European Mesolithic hunter-gatherers. Since they occupied a completely different niche, the UK representatives simply had nothing to share with HV and JT.

The best example of mitoconflict is the 5-year-old conflict between two brilliant minds in amateur genetics and anthropology - Dienek Pontikos (whose mitogroup is T2) and David "Polako" Veselovsky (whose mitogroup is H7). This is not confirmation of the conflict potential of interaction between the JT and HV mitogroups. This is like the well-known experiment with 1 g of iron powder or powder and 2 g of dry potassium nitrate, previously ground in a mortar. As soon as they are placed next to each other, a violent reaction begins with the release of sparks, brownish smoke and strong heating. In this case, the appearance of the mixture resembles red-hot lava. When potassium nitrate reacts with iron, potassium ferrate and gaseous nitrogen monoxide are formed, which, when oxidized in air, produces brown gas - nitrogen dioxide. If the solid residue after the end of the reaction is placed in a glass of cold boiled water, you will get a red-violet solution of potassium ferrate, which decomposes in a few minutes.))

What are the practical consequences of these observations? Currently, one of the branches of the so-called conflictology, associated with assessing the compatibility of individuals in a group, is rapidly developing. Naturally, this industry receives its most practical expression in solving practical problems (for example, casting or personnel selection). Of course, recruited personnel are assessed mainly on their professional knowledge, skills, abilities and work experience. But an important factor is assessing the compatibility of recruits with the already established team and management. An a priori assessment of this factor is difficult, and now this assessment is made mainly with the help of psychological tests, on the development and testing of which large corporations and institutions (for example, NASA when selecting a team of astronauts) spend large amounts of money. However, now, on the threshold of the development of psychogenetics, these tests can be replaced by an analysis of genetically determined compatibility.

For example, suppose that we have a certain group of recruited specialists who meet the formal requirements for employment and have the appropriate competence. There is a team in which, say, all three macrogroups JT, HV are presentand UK. If I were a manager, then new recruits would be assigned to certain groups of people based on the assigned tasks:

1) If the implementation of a certain task requires the presence of a close group of like-minded people, then the best option is to create a group of people belonging to the same macrohaplogroup
2) If the group is working towards finding new solutions and uses methods such as “brainstorming” in its work, it is necessary to place these recruits in the environment of antagonists (JT to HV, and vice versa)

3) If the principles of the group’s work are based purely on business/formal relations, then management should ensure that the group has a sufficient number of UK representatives who will act as a buffer between conflicting JTs and HVs.

If desired, the same principles can be used as the basis for “scientifically motivated” selection of a marriage partner. At the very least, assessing a partner’s compatibility (or rather, assessing the nature of compatibility) will be much more plausible than assessing compatibility in modern dating services, which is based on primitive psychological tests and astrology.K By the way, the only commercial DNA dating service strictly exploits the haplotypes of the histocompatibility complex. The logic is that, as scientists have shown, people usually choose partners with the most opposite HLA haplotype.

Different genetic components in the Norwegian population revealed by the analysis of mtDNA & Y chromosome polymorphisms Mitochondrial DNA haplogroups influence AIDS progression.

Mitochondrion: 30 Mitochondrial haplogroup T is associated with coronary artery disease Mitochondrial DNA haplotype ‘T’ carriers are less prone to diabetes « Mathilda’s Anthropology Blog

“Elsewhere it has been reported that membership in haplogroup T may offer some protection against Alexander Belovzheimer Disease (Chagnon et al. 1999; Herrnstadt et al. 2002) and also Parkinson's Disease (Pyle et al. 2005), but the cautionary words of Pereira et al. suggest that further studies may be necessary before reaching firm conclusions."

Mitochondrial DNA haplogroups influence AIDS progression.

Natural selection shaped regional mtDNA variation in humans
Ruiz-Pesini E, Lapeña AC, Díez-Sánchez C, et al. (September 2000). "Human mtDNA haplogroups associated with high or reduced spermatozoa motility." Am. J.Hum. Genet. 67(3):682–96. DOI:10.1086/303040. PMID 10936107.
Mitochondrion: 30 Mitochondrial haplogroup T is associated with coronary artery disease
Mitochondrial DNA haplotype ‘T’ carriers are less prone to diabetes « Mathilda’s Anthropology Blog
“Elsewhere it has been reported that membership in haplogroup T may offer some protection against

05.05.2015 13.10.2015

All information about the structure of the human body and its predisposition to diseases is encrypted in the form of DNA molecules. The main information is located in the cell nuclei. However, 5% of DNA is localized in mitochondria.

What are mitochondria called?

Mitochondria are cellular organelles of eukaryotes that are needed in order to convert the energy contained in nutrients into compounds that can be absorbed by cells. Therefore, they are often called “energy stations”, because without them the existence of the body is impossible.
These organelles acquired their own genetic information due to the fact that they were previously bacteria. After they entered the cells of the host organism, they were unable to retain their genome, while they transferred part of their own genome to the cell nucleus of the host organism. Therefore, now their DNA (mtDNA) contains only a part, namely 37 genes, of the original amount. Mainly, they encrypt the mechanism of transformation of glucose into compounds - carbon dioxide and water with the production of energy (ATP and NADP), without which the existence of the host organism is impossible.

What is unique about mtDNA?

The main property inherent in mitochondrial DNA is that it can be inherited only through the mother's line. In this case, all children (men or women) can receive mitochondria from the egg. This happens due to the fact that female eggs contain a higher number of these organelles (up to 1000 times) than male sperm. As a result, the daughter organism receives them only from its mother. Therefore, their inheritance from the paternal cell is completely impossible.
It is known that mitochondrial genes were passed on to us from the distant past - from our promother - “mitochondrial Eve”, who is the common ancestor of all people on the planet on the maternal side. Therefore, these molecules are considered the most ideal object for genetic examinations to establish maternal kinship.

How is kinship determined?

Mitochondrial genes have many point mutations, making them highly variable. This allows us to establish kinship. During genetic examination, using special genetic analyzers - sequencers, individual point nucleotide changes in the genotype, their similarity or difference, are determined. In people who are not related on their mother's side, the mitochondrial genomes differ significantly.
Determining kinship is possible thanks to the amazing characteristics of the mitochondrial genotype:
they are not subject to recombination, so molecules change only through the process of mutation, which can occur over a millennium;
possibility of isolation from any biological materials;
if there is a lack of biomaterial or degradation of the nuclear genome, mtDNA can become the only source for analysis due to the huge number of its copies;
Due to the large number of mutations compared to the nuclear genes of cells, high accuracy is achieved when analyzing genetic material.

What can be determined through genetic testing?

Genetic testing of mtDNA will help in diagnosing the following cases.
1. To establish kinship between people on the mother’s side: between a grandfather (or grandmother) and a grandson, a brother and sister, an uncle (or aunt) and a nephew.
2. When analyzing a small amount of biomaterial. After all, each cell contains mtDNA in significant quantities (100 - 10,000), while nuclear DNA contains only 2 copies for each 23 chromosomes.
3. When identifying ancient biomaterial – a shelf life of more than a thousand years. It is thanks to this property that scientists were able to identify genetic material from the remains of members of the Romanov family.
4. In the absence of other material, even one hair contains a significant amount of mtDNA.
5. When determining the belonging of genes to the genealogical branches of humanity (African, American, Middle Eastern, European haplogroup and others), thanks to which it is possible to determine the origin of a person.

Mitochondrial diseases and their diagnosis

Mitochondrial diseases manifest themselves mainly due to defects in the mtDNA of cells associated with a significant susceptibility of these organelles to mutations. Today there are already about 400 diseases associated with their defects.
Normally, each cell can include both normal mitochondria and those with certain disorders. Often, signs of the disease do not manifest themselves at all. However, when the process of energy synthesis weakens, the manifestation of such diseases is observed in them. These diseases are primarily associated with disorders of the muscular or nervous systems. As a rule, with such diseases there is a late onset of clinical manifestations. The incidence of these diseases is 1:200 people. It is known that the presence of mitochondrial mutations can cause nephrotic syndrome during pregnancy and even sudden death of the infant. Therefore, researchers are making active attempts to solve these problems associated with the treatment and transmission of genetic diseases of this type from mothers to children.

How is aging related to mitochondria?

Reorganization of the genome of these organelles was also discovered when analyzing the mechanism of aging of the body. Researchers at Hopkins University published results from monitoring the blood levels of 16,000 elderly American people, demonstrating that the decrease in the amount of mtDNA was directly related to the age of the patients.

Most of the issues considered today have become the basis of a new science - “mitochondrial medicine”, which was formed as a separate direction in the 20th century. Prediction and treatment of diseases associated with mitochondrial genome disorders, genetic diagnostics are its primary tasks.

What is mitochondrial DNA?

Mitochondrial DNA (mtDNA) is DNA located in mitochondria, cellular organelles inside eukaryotic cells that convert chemical energy from food into a form that cells can use - adenosine triphosphate (ATP). Mitochondrial DNA represents only a small part of the DNA in a eukaryotic cell; Most DNA can be found in the cell nucleus, in plants and algae, and in plastids such as chloroplasts.

In humans, the 16,569 base pairs of mitochondrial DNA encode just 37 genes. Human mitochondrial DNA was the first significant portion of the human genome to be sequenced. In most species, including humans, mtDNA is inherited only from the mother.

Because animal mtDNA evolves faster than nuclear genetic markers, it represents the basis of phylogenetics and evolutionary biology. This has become an important point in anthropology and biogeography, as it allows one to study the interrelationships of populations.

Hypotheses for the origin of mitochondria

Nuclear and mitochondrial DNA are believed to have different evolutionary origins, with mtDNA derived from the circular genomes of bacteria that were absorbed by the early ancestors of modern eukaryotic cells. This theory is called the endosymbiotic theory. It is estimated that each mitochondrion contains copies of 2-10 mtDNA. In the cells of living organisms, the vast majority of the proteins present in mitochondria (numbering about 1,500 different types in mammals) are encoded by nuclear DNA, but the genes for some, if not most, of these are thought to be originally bacterial and have since been transferred to the eukaryotic nucleus. during evolution.

The reasons why mitochondria retain certain genes are discussed. The existence of genome-less organelles in some species of mitochondrial origin suggests that complete gene loss is possible, and the transfer of mitochondrial genes to the nucleus has a number of advantages. The difficulty of orienting remotely produced hydrophobic protein products in mitochondria is one hypothesis for why some genes are retained in mtDNA. Co-localization for redox regulation is another theory, citing the desirability of localized control of mitochondrial machinery. Recent analysis of a wide range of mitochondrial genomes suggests that both of these functions may dictate mitochondrial gene retention.

Genetic examination of mtDNA

In most multicellular organisms, mtDNA is inherited from the mother (maternal lineage). Mechanisms for this include simple dilution (an egg contains an average of 200,000 mtDNA molecules, whereas healthy human sperm contains an average of 5 molecules), degradation of sperm mtDNA in the male reproductive tract, in the fertilized egg, and, in at least a few organisms, failure The mtDNA of the sperm penetrates into the egg. Whatever the mechanism, it is unipolar inheritance - inheritance of mtDNA, which occurs in most animals, plants and fungi.

Maternal inheritance

In sexual reproduction, mitochondria are usually inherited exclusively from the mother; mitochondria in mammalian sperm are usually destroyed by the egg after fertilization. Additionally, most mitochondria are present at the base of the sperm tail, which is used for sperm cell movement; sometimes the tail is lost during fertilization. In 1999, it was reported that paternal sperm mitochondria (containing mtDNA) are marked by ubiquitin for subsequent destruction within the embryo. Some in vitro fertilization methods, particularly sperm injection into the oocyte, may interfere with this.

The fact that mitochondrial DNA is inherited through the maternal line allows genealogical researchers to trace the maternal line far back in time. (Y-chromosomal DNA is paternally inherited, used in a similar way to determine patrilineal history.) This is usually done on a person's mitochondrial DNA by sequencing the hypervariable control region (HVR1 or HVR2), and sometimes the entire mitochondrial DNA molecule as a DNA genealogy test. For example, HVR1 consists of approximately 440 base pairs. These 440 pairs are then compared to control regions of other individuals (or specific individuals or subjects in the database) to determine maternal lineage. The most common comparison is with the Revised Cambridge Reference Sequence. Vilà et al. published studies on the matrilineal similarity of domestic dogs and wolves. The concept of Mitochondrial Eve is based on the same type of analysis, attempts to discover the origins of humanity, traces the origin back in time.

mtDNA is highly conserved, and its relatively slow mutation rates (compared to other regions of DNA such as microsatellites) make it useful for studying evolutionary relationships—the phylogeny of organisms. Biologists can determine and then compare mtDNA sequences across species and use the comparisons to construct an evolutionary tree for the species studied. However, due to the slow mutation rates it experiences, it is often difficult to distinguish closely related species to any extent, so other methods of analysis must be used.

Mitochondrial DNA mutations

Individuals undergoing unidirectional inheritance and little or no recombination can be expected to undergo Müllerian ratchet, the accumulation of deleterious mutations until functionality is lost. Animal mitochondrial populations avoid this accumulation due to a developmental process known as the mtDNA bottleneck. The bottleneck uses stochastic processes in the cell to increase cell-to-cell variability in mutant load as the organism develops, such that one egg cell with some proportion of mutant mtDNA creates an embryo in which different cells have different mutant loads. The cellular level can then be targeted to remove these cells with more mutant mtDNA, resulting in stabilization or reduction of the mutant load between generations. The mechanism underlying the bottleneck is discussed with recent mathematical and experimental metastasis and provides evidence for a combination of random partitioning of mtDNA into cell divisions and random turnover of mtDNA molecules within the cell.

Paternal inheritance

Double unidirectional inheritance of mtDNA is observed in bivalves. In these species, females have only one type of mtDNA (F), whereas males have type F mtDNA in their somatic cells, but M type mtDNA (which can be up to 30% divergent) in germline cells. Maternally inherited mitochondria have additionally been reported in some insects such as fruit flies, bees, and periodical cicadas.

Male mitochondrial inheritance was recently discovered in Plymouth Rock chickens. Evidence supports rare cases of male mitochondrial inheritance in some mammals. In particular, documented cases exist for mice where male-derived mitochondria were subsequently rejected. Additionally, it has been found in sheep and also in cloned cattle. Once found in a man's body.

Although many of these cases involve embryo cloning or subsequent rejection of paternal mitochondria, others document inheritance and persistence in vivo in vitro.

Mitochondrial donation

IVF, known as mitochondrial donation or mitochondrial replacement therapy (MRT), results in offspring containing mtDNA from female donors and nuclear DNA from the mother and father. In the spindle transfer procedure, an egg nucleus is introduced into the cytoplasm of an egg from a female donor that has had the nucleus removed but still contains the mtDNA of the female donor. The composite egg is then fertilized by the man's sperm. This procedure is used when a woman with genetically defective mitochondria wants to produce offspring with healthy mitochondria. The first known child to be born as a result of mitochondrial donation was a boy born to a Jordanian couple in Mexico on April 6, 2016.

Mitochondrial DNA structure

In most multicellular organisms, mtDNA - or the mitogenome - is organized as round, circularly closed, double-stranded DNA. But in many unicellular organisms (for example, tetrahymena or the green alga Chlamydomonas reinhardtii) and in rare cases in multicellular organisms (for example, some species of cnidarians), mtDNA is found as linearly organized DNA. Most of these linear mtDNAs possess telomerase-independent telomeres (i.e., the ends of the linear DNA) with different modes of replication, which have made them interesting subjects of study, since many of these single-celled organisms with linear mtDNA are known pathogens.

For human mitochondrial DNA (and probably for metazoans), 100-10,000 individual copies of mtDNA are typically present in a somatic cell (eggs and sperm are exceptions). In mammals, each double-stranded circular mtDNA molecule consists of 15,000-17,000 base pairs. The two strands of mtDNA differ in their nucleotide content, the guanide-rich strand is called the heavy chain (or H-strand) and the cynosine-rich strand is called the light chain (or L-strand). The heavy chain encodes 28 genes and the light chain encodes 9 genes, for a total of 37 genes. Of the 37 genes, 13 are for proteins (polypeptides), 22 are for transferring RNA (tRNA), and two are for small and large subunits of ribosomal RNA (rRNA). The human mitogenome contains overlapping genes (ATP8 and ATP6, and ND4L and ND4: see Human genome map of mitochondria), which is rare in animal genomes. The 37-gene pattern is also found among most metazoans, although, in some cases, one or more of these genes are missing and the range of mtDNA sizes is greater. Even greater variation in the content and size of mtDNA genes exists among fungi and plants, although there appears to be a core subset of genes that is present in all eukaryotes (except for the few that have no mitochondria at all). Some plant species have huge mtDNA (as much as 2,500,000 base pairs per mtDNA molecule), but surprisingly, even these huge mtDNA contain the same number and types of genes as related plants with much smaller mtDNA.

The cucumber (Cucumis Sativus) mitochondrial genome consists of three circular chromosomes (length 1556, 84 and 45 kb), which are completely or largely autonomous with respect to their replication.

Six major genome types are found in mitochondrial genomes. These types of genomes were classified by "Kolesnikov and Gerasimov (2012)" and differ in various ways, such as circular versus linear genome, genome size, presence of introns or plasmid-like structures, and whether the genetic material is a distinct molecule, a collection of homogeneous or heterogeneous molecules.

Decoding the animal genome

In animal cells, there is only one type of mitochondrial genome. This genome contains one circular molecule between 11-28 kbp of genetic material (type 1).

Decoding the plant genome

There are three different types of genome found in plants and fungi. The first type is a circular genome that has introns (type 2) ranging from 19 to 1000 kbp in length. The second type of genome is a circular genome (about 20-1000 kbp), which also has a plasmid structure (1kb) (type 3). The final type of genome that can be found in plants and fungi is the linear genome, consisting of homogeneous DNA molecules (type 5).

Decoding the protist genome

Protists contain a wide variety of mitochondrial genomes, which include five different types. Type 2, type 3 and type 5, mentioned in plant and fungal genomes, also exist in some protozoa, as well as in two unique genome types. The first of these is a heterogeneous collection of circular DNA molecules (type 4), and the final genome type found in protists is a heterogeneous collection of linear molecules (type 6). Genome types 4 and 6 range from 1 to 200 kb.

Endosymbiotic gene transfer, the process of genes encoded in the mitochondrial genome being carried primarily by the cell's genome, likely explains why more complex organisms, such as humans, have smaller mitochondrial genomes than simpler organisms, such as protozoa.

Mitochondrial DNA replication

Mitochondrial DNA is replicated by the DNA polymerase gamma complex, which consists of a 140 kDa catalytic DNA polymerase encoded by the POLG gene and two 55 kDa accessory subunits encoded by the POLG2 gene. The replication apparatus is formed by DNA polymerase, TWINKLE and mitochondrial SSB proteins. TWINKLE is a helicase that unwinds short stretches of dsDNA in the 5" to 3" direction.

During embryogenesis, mtDNA replication is tightly regulated from the fertilized oocyte through the preimplantation embryo. Effectively reducing the number of cells in each cell, mtDNA plays a role in the mitochondrial bottleneck, which exploits cell-to-cell variability to improve the inheritance of damaging mutations. At the blastocyte stage, the onset of mtDNA replication is specific to trophtocoder cells. In contrast, cells of the inner cell mass restrict mtDNA replication until they receive signals to differentiate into specific cell types.

Mitochondrial DNA transcription

In animal mitochondria, each strand of DNA is continuously transcribed and produces a polycistronic RNA molecule. There are tRNAs present between most (but not all) protein-coding regions (see Map of the Human Mitochondria Genome). During transcription, tRNA acquires a characteristic L-form, which is recognized and cleaved by specific enzymes. When mitochondrial RNA is processed, individual fragments of mRNA, rRNA, and tRNA are released from the primary transcript. Thus, folded tRNAs act as minor punctuations.

Mitochondrial diseases

The concept that mtDNA is particularly susceptible to reactive oxygen species generated by the respiratory chain due to its proximity remains controversial. mtDNA does not accumulate more oxidative base than nuclear DNA. It has been reported that at least some types of oxidative DNA damage are repaired more efficiently in mitochondria than in the nucleus. mtDNA is packaged with proteins that appear to be as protective as nuclear chromatin proteins. Moreover, mitochondria have evolved a unique mechanism that maintains mtDNA integrity by degrading excessively damaged genomes followed by replication of intact/repaired mtDNA. This mechanism is absent in the nucleus and is activated by several copies of mtDNA present in mitochondria. The result of a mutation in mtDNA can be a change in the coding instructions for certain proteins, which can affect the metabolism and/or fitness of the organism.

Mitochondrial DNA mutations can lead to a number of diseases, including exercise intolerance and Kearns-Sayre syndrome (KSS), which causes a person to lose full function of heart, eye and muscle movements. Some evidence suggests that they may be a significant contributor to the aging process and age-related pathologies. Specifically, in the context of disease, the proportion of mutant mtDNA molecules in a cell is called heteroplasm. The distributions of heteroplasm within and between cells dictate the onset and severity of disease and are influenced by complex stochastic processes within the cell and during development.

Mutations in mitochondrial tRNAs may be responsible for severe diseases such as MELAS and MERRF syndromes.

Mutations in nuclear genes encoding proteins that use mitochondria can also contribute to mitochondrial diseases. These diseases do not follow mitochondrial inheritance patterns, but instead follow Mendelian patterns of inheritance.

Recently, mutations in mtDNA have been used to help diagnose prostate cancer in biopsy-negative patients.

Mechanism of aging

Although the idea is controversial, some evidence suggests a link between aging and mitochondrial dysfunction in the genome. Essentially, mutations in mtDNA disrupt the careful balance of reactive oxygen production (ROS) and enzymatic ROS production (by enzymes such as superoxide dismutase, catalase, glutathione peroxidase, and others). However, some mutations that increase ROS production (for example, by reducing antioxidant defenses) in worms increase, rather than decrease, their longevity. In addition, nude moth rats, rodents the size of mice, live approximately eight times longer than mice, despite having decreased antioxidant defenses and increased oxidative damage to biomolecules compared to mice.

At one point there was believed to be a virtuous feedback loop at work ("Vicious Cycle"); as mitochondrial DNA accumulates genetic damage caused by free radicals, mitochondria lose function and release free radicals in the cytosol. Decreased mitochondrial function reduces overall metabolic efficiency. However, this concept was finally refuted when it was demonstrated that mice genetically modified to accumulate mtDNA mutations at an increased rate age prematurely, but their tissues do not produce more ROS, as predicted by the "Vicious Cycle" hypothesis. Supporting the link between longevity and mitochondrial DNA, some studies have found correlations between the biochemical properties of mitochondrial DNA and species longevity. Extensive research is being conducted to further explore this connection and anti-aging treatments. Currently, gene therapy and nutraceutical supplements are popular areas of ongoing research. Bjelakovic et al. analyzed the results of 78 studies between 1977 and 2012, involving a total of 296,707 participants, and concluded that antioxidant supplements did not reduce mortality from any cause or prolong life expectancy, while some of these, such as beta-carotene, vitamin E and higher doses of vitamin A, may actually increase mortality.

Deletion breakpoints often occur within or adjacent to regions exhibiting non-canonical (non-B) conformations, namely hairpin, cross, and clover-like elements. In addition, there is evidence that helical distortion curvilinear regions and long G-tetrads are involved in detecting instability events. In addition, higher density points were consistently observed in regions with GC skew and in close proximity to the degenerate sequence fragment YMMYMNNMMHM.

How is mitochondrial DNA different from nuclear DNA?

Unlike nuclear DNA, which is inherited from both parents and in which genes are rearranged through the process of recombination, there is usually no change in mtDNA from parent to offspring. Although mtDNA also recombines, it does so with copies of itself within the same mitochondrion. Because of this, the mutation rate of animal mtDNA is higher than that of nuclear DNA. mtDNA is a powerful tool for tracing matrilineage and has been used in this role to trace the ancestry of many species hundreds of generations ago.

The rapid rate of mutation (in animals) makes mtDNA useful for assessing the genetic relationships of individuals or groups within a species, and for identifying and quantifying phylogenies (evolutionary relationships) among different species. To do this, biologists determine and then compare the mtDNA sequence from different individuals or species. Data from the comparisons are used to construct a network of relationships between sequences that provide an estimate of the relationships between the individuals or species from which the mtDNA was taken. mtDNA can be used to assess relationships between closely related and distant species. Due to the high frequency of mtDNA mutations in animals, 3rd position codons change relatively quickly, and thus provide information about genetic distances between closely related individuals or species. On the other hand, the substitution rate of mt proteins is very low, so amino acid changes accumulate slowly (with corresponding slow changes in 1st and 2nd codon positions) and thus they provide information about the genetic distances of distant relatives. Statistical models that consider substitution rates among codon positions separately can therefore be used to simultaneously estimate phylogenies that contain both closely related and distant species.

History of the discovery of mtDNA

Mitochondrial DNA was discovered in the 1960s by Margit M. K. Nas and Silvan Nas using electron microscopy as DNase-sensitive strands within mitochondria, and by Ellen Hasbrunner, Hans Tappi and Gottfried Schatz from biochemical analyzes on highly purified mitochondrial fractions.

Mitochondrial DNA was first recognized in 1996 during Tennessee v. Paul Ware. In 1998, in the court case Commonwealth of Pennsylvania v. Patricia Lynn Rorrer, mitochondrial DNA was admitted into evidence for the first time in the State of Pennsylvania. The case was featured in Episode 55 of Season 5 of the True Drama Forensic Court Case Series (Season 5).

Mitochondrial DNA was first recognized in California during the successful prosecution of David Westerfield for the 2002 kidnapping and murder of 7-year-old Danielle van Dam in San Diego, and has been used to identify both humans and dogs. This was the first test in the US to resolve canine DNA.

mtDNA databases

Several specialized databases have been created to collect mitochondrial genome sequences and other information. Although most of them focus on sequence data, some include phylogenetic or functional information.

MitoSatPlant: microsatellite database of mitochondrial viridiplants.

MitoBreak: Mitochondrial DNA Breakpoint Database.

MitoFish and MitoAnnotator: fish mitochondrial genome database. See also Cawthorn et al.

MitoZoa 2.0: database for comparative and evolutionary analysis of mitochondrial genomes (no longer available)

InterMitoBase: an annotated database and protein-protein interaction analysis platform for human mitochondria (last updated in 2010, but still not available)

Mitome: database for comparative mitochondrial genomics in metazoans (no longer available)

MitoRes: a resource for nuclear-encoded mitochondrial genes and their products in metazoans (no longer updated)

There are several specialized databases that report polymorphisms and mutations in human mitochondrial DNA along with assessments of their pathogenicity.

MITOMAP: a compendium of polymorphisms and mutations in human mitochondrial DNA.

MitImpact: Collection of predicted pathogenicity predictions for all nucleotide changes that cause nonsynonymous substitutions in human mitochondrial protein-coding genes.

Magnetic fields are physical and external forces that cause multiple reactions in cell biology, which include changes in the exchange of information in RNA and DNA, as well as many genetic factors. When changes occur in the planetary magnetic field, the level of electromagnetism (EMF) changes, directly altering cellular processes, genetic expression and blood plasma. The functions of proteins in the human body, as well as in the blood plasma, are associated with the properties and influence of the EMF field. Proteins perform a variety of functions in living organisms, including acting as catalysts for metabolic reactions, replicating DNA, triggering responses to pathogens, and moving molecules from one place to another. Blood plasma acts as a protein storehouse in the body, protecting against infection and disease, and plays a vital role in providing proteins needed for DNA synthesis. The quality of our blood and blood plasma is what gives commands to the entire body of proteins, expressed through our genetic material in all cells and tissues. This means that the blood directly interacts with the body through proteins, which has been encoded in our DNA. This protein synthesis connection between DNA, RNA and mitochondria of cells changes as a result of changes in the magnetic field.

In addition, our red blood cells contain hemoglobin, which is a protein based on four iron atoms associated with the state of the iron core and the magnetism of the Earth. Hemoglobin in the blood carries oxygen from the lungs to the rest of the body, where the oxygen is released to burn nutrients. This provides energy for our body to function in a process called energy metabolism. This is important because changes in our blood are directly related to the energy in the metabolic process in our body and mind. This will become even more apparent as we begin to pay attention to these signs that are changing energy consumption and the use of energy resources on the planet. Returning them to their rightful owner also means changing the energy metabolism in the microcosm of our body, reflecting changes in the macrocosm of the Earth. This is an important stage of ending the consumptive modeling of the Controllers in order to achieve a balance of conservation principles in order to find internal balance, and therefore achieve energetic balance within these systems. An important part of these changes lies in the mystery of the higher functions of the mitochondria.

Mother's Mitochondrial DNA

When we compare the gender principle inherent in our creation and the fact that our Mother principle returns energetic balance to the earth's core through the magnetic field, the next step is the restoration of mitochondrial DNA. Mitochondrial DNA is DNA located in mitochondria, structures inside cells that convert chemical energy from food into a form that cells can use, adenosine triphosphate (ATP). ATP measures the light coefficient conducted by the cells and tissues of the body and is directly related to the embodiment of spiritual consciousness, which is energy and is important for energy metabolism.

Mitochondrial DNA is only a small part of the DNA in a cell; Most of the DNA is contained in the cell nucleus. In most species on Earth, including humans, mitochondrial DNA is inherited exclusively from the mother. Mitochondria have their own genetic material and machinery to create their own RNA and new proteins. This process is called protein biosynthesis. Protein biosynthesis refers to the processes by which biological cells generate new sets of proteins.

Without properly functioning mitochondrial DNA, humanity cannot efficiently produce new proteins for DNA synthesis, nor maintain the level of ATP needed to generate light within the cell to embody our spiritual consciousness. Thus, due to damage to mitochondrial DNA, humanity has become extremely addicted to consuming everything in the outside world to fill the energetic void within our cells. (See Alien NAA installations for addictions).

Without knowing anything different about our recent history and having erased memories, humanity is unaware that we existed with a significantly dysfunctional mitochondrion.

This is a direct result of the extraction of Mother's DNA, magnetic principles, proton structure from the Earth and the presence of a synthetic alien version of the "Dark Mother" that was placed into the planetary architecture to emulate her functions. Humanity existed on the planet without its true Mother Principle, and this was apparently written into the cells of our mitochondrial DNA. This has been described many times as the NAA invading the Planetary Logos through the manipulation of the magnetosphere and magnetic field.

Krista

The inner mitochondrial membrane is distributed in numerous cristae, which increase the surface area of the inner mitochondrial membrane, increasing its ability to produce ATP. It is this region of the mitochondria, when functioning correctly, that increases ATP energy and generates light in the cells and tissues of the body. The higher function of the cristae in the mitochondrion is activated in the Ascension groups beginning in this cycle. The name "crista" was given as a result of a scientific discovery because it is directly related to the activation of the crystal gene.

Changes in estrogen receptors

Maternal mitochondrial DNA and magnetic shifts have many factors that make adjustments and cause symptoms in women's reproductive cycles. Estrogen hormones activate estrogen receptors, which are proteins found in cells that bind to DNA, causing changes in genetic expression. Cells can communicate with each other by releasing molecules that transmit signals to other receptive cells. Estrogen is released by tissues such as the ovaries and placenta, passing through the cell membranes of receiving cells and binding to estrogen receptors in the cells. Estrogen receptors control the transmission of messages between DNA and RNA. Thus, nowadays, many women are noticing unusual, strange menstrual cycles caused by estrogen dominance. Changes in estrogen levels occur in both men and women, so listen to your body to help support these changes. Take care of your liver and detoxification, eliminate sugar consumption and foods that stimulate and increase hormones, monitor the bacterial balance in the intestines and body - this is useful for maintaining estrogen balance.

Mitochondrial disease drains energy

Mitochondrial diseases result from genetic mutations imprinted in the DNA sequence. Artificial architecture placed on a planet, such as alien mechanisms seeking to create genetic modifications to usurp Mother DNA, which manifest as mutations and DNA damage of all kinds. Mitochondrial diseases are characterized by blockage of energy in the body due to the fact that the disease accumulates, inheriting maternal genetics in hereditary bloodlines.

The mitochondria is important for the daily functioning of cells and energy metabolism, which also leads to the spiritual development of the soul and the embodiment of the Oversoul (monad). Mitochondrial disease reduces the effective generation of energy available to the body and mind, stunting human development and spiritual growth. Thus, the body ages faster and the risk of disease increases; personal energy is deactivated and thus exhausted. This significantly limits the amount of usable energy available for brain development and the functioning of all neurological systems. Depletion of energy reserves for brain and neurological development contributes to the spectrum of autism, neurodegeneration and other brain deficiencies. Defects in mitochondrial genes are associated with hundreds of “clinical” blood, brain and neurological disorders.

The blood, brain and neurological functions of the planetary body are equated with the architecture of the ley lines, chakra centers and Star Gate systems that control the energy flow (blood) to form the body of consciousness known as the Tree Network of the 12 Planetary Temple. The blood, brain and neurological functions of the human body are equated to the same Tree Network 12 of the Human Temple. Once the Temple and DNA installations are damaged or altered, the blood, brain and nervous system are damaged. If our blood, brain and nervous system are blocked or damaged, we cannot translate language, communicate with, build multidimensional light bodies to receive higher wisdom (Sophia). Our kinds of language on many levels, including our DNA language, are confused and mixed by those who sought to enslave and brutalize the Earth.

As we know, most sources of kinetic or other external energies are actively controlled by the power elite to suppress human development and limit the opportunities for equitable use or fair exchange of resources for shared use by the Earth's population. The strategy is to control all energy and energy sources (even control of DNA and soul), thus creating a ruling class and a class of slaves or slaves. Using the Orion group's "divide and conquer" method, it is much easier to control a population that is traumatized by fear, ignorant and in poverty.

Translation: Oreanda Web