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Clusters of human body cells have different genomes

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From a study of samples collected from 500 people:

The human body is a complex mosaic made up of clusters of cells with different genomes — and many of these clusters bear mutations that could contribute to cancer, according to a sweeping survey of 29 different types of tissue…

Overall, the study found fewer examples of mosaicism in some types of tissue than would be expected on the basis of previous research. But the key, says Martincorena, is that the latest analysis demonstrated that mosaicism is present across a wide array of tissues.

Tissues with a high rate of cell division, such as those that make up the skin and oesophagus, tended to have more mosaicism than tissues with lower rates of cell division. Mosaicism also increased with age, and was particularly prevalent in the lungs and skin — tissues that are exposed to environmental factors that can damage DNA.

Heidi Ledford, “The human body is a mosaic of different genomes” at Nature

Remember the Selfish Gene? Aw, he was just playin’ you guys. You didn’t fall for that, did you?

See also: Researchers’ new find: Liver, pancreas cells are generally as old as the brain If the vast majority of liver cells are as old as the animal, being kind to the liver may be a key to longevity. It will be interesting to see whether epigenetic changes affect new cells or old cells more.

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Mimus *crickets chirping*. @OLV: do not bother. Un-intelligent brains produced via mindless processes can not grasp the sheer complexity of the stomatal closure/feedback system. Your Humpty Dumpty was glorious :) Long death to darwinism! Truthfreedom
Here’s a question that was posted in ResearchGate: Is it realistic for a physicist to become a biologist? I work in material science (specializing in TEM microscopy and magnetism). Right now I'm finishing my Ph.D. I'm very interested in biology (topics like programmed cell death and ageing), however I have doubts whether it's realistic at this point to change my career path. Here’s one of the responses: Absolutely. Especially, if you want to specialize in Computational and Systems Biology, Integrative Biology, Biophotonics, Biophysics etc. But, not necessary, I know many people in Physics who went to Cell Biology, Molecular Biology, Microbiology, etc, and were very successful. Are there examples of people switching careers in the opposite direction, ie from biology to physics? Just curious. OLV
Our research underscores the importance of feedback regulation in generating robust and adaptable biological responses. The high validation rate of our model illustrates the advantages of discrete dynamic modeling for complex, nonlinear systems common in biology. A new discrete dynamic model of ABA-induced stomatal closure predicts key feedback loops PLoS Biol. 2017 Sep; 15(9): e2003451. Published online 2017 Sep 22. doi: 10.1371/journal.pbio.2003451 PMCID: PMC5627951 PMID: 28937978 OLV
Stomata, microscopic pores in leaf surfaces through which water loss and carbon dioxide uptake occur, are closed in response to drought by the phytohormone abscisic acid (ABA). This process is vital for drought tolerance and has been the topic of extensive experimental investigation in the last decades. Although a core signaling chain has been elucidated consisting of ABA binding to receptors, which alleviates negative regulation by protein phosphatases 2C (PP2Cs) of the protein kinase OPEN STOMATA 1 (OST1) and ultimately results in activation of anion channels, osmotic water loss, and stomatal closure, over 70 additional components have been identified, yet their relationships with each other and the core components are poorly elucidated. A new discrete dynamic model of ABA-induced stomatal closure predicts key feedback loops PLoS Biol. 2017 Sep; 15(9): e2003451. Published online 2017 Sep 22. doi: 10.1371/journal.pbio.2003451 PMCID: PMC5627951 PMID: 28937978 OLV
Mimus, This decade-old information may provide some valuable hints: Hope for Humpty Dumpty: Systems Biology of Cellular Signaling Sarah M. Assmann Humpty Dumpty, a traditional English nursery rhyme: Humpty Dumpty sat on a wall, Humpty Dumpty had a great fall. All the king's horses, And all the king's men, Couldn't put Humpty together again. One definition of systems biology is the modeling of the relationships, or networks, within and/or between large-scale data sets. As scientists' knowledge of living systems has grown, it has become increasing difficult to understand relationships between all the components of a biological network by intuitive approaches alone. The value of systems biology is that it (1) helps us to organize information about complex systems; (2) reveals hidden content, or “emergent properties,” of the system that would not be deduced from a study of the separate parts of the system; and (3) provides predictions of how the system would behave under conditions that have not yet been observed. Such predictions can then be used to inform and direct wet bench experiments. OLV
Mimus, Let’s make it easier. You may point to the scientific literature that coherently and comprehensively explains it. I’ll have someone verify it. Thanks. OLV
Mimus, Since you seem very knowledgeable about biology, would you kindly tell us if -as far as you’re aware of- any living human being knows how we could have gotten the transposons, the prokaryotic cell, the eukaryotic cell? I’m sure many readers would highly appreciate you sharing such a valuable knowledge here. OLV
God what a load of rubbish. What on earth does this have to do with the selfish gene? And what is pav on about? Some mutations aren't transmitted so natural selection doesn't work? Really? EDTA's question is at least sensible, but the answer is no. Direct estimates of the mutation rate use multiple tissues to avoid counting somatic mutations, and indirect ones aggregate over so many generations that the possibility of somatic mutations in the last gen only adds a little noise. Mimus
Activation of transposable elements and genetic instability during long-term culture of the human fungal pathogen Candida albicans Leszek Potocki . Ewelina Kuna . Kamila Filip . Beata Kasprzyk . Anna Lewinska . Maciej Wnuk Biogerontology https://doi.org/10.1007/s10522-019-09809-2 It has been repeatedly reported that trans- posable elements (TE) become active and/or mobile in the genomes of replicatively and stress-induced senescent mammalian cells. However, the biological role of senescence-associated transposon activation and its occurrence and relevance in other eukaryotic cells remain to be elucidated. In the present study, Candida albicans, a prevalent opportunistic fungal pathogen in humans, was used to analyze changes in gene copy number of selected TE, namely Cirt2, Moa and Cmut1 during long-term culture (up to 90 days). The effects of stress stimuli (fluconazole, hydrogen peroxide, hypochlorite) and ploidy state (haploid, diploid, tetraploid cells) were also considered. An increase in copy number of Cirt2 and Moa was the most accented in tetraploid cells after 90 days of culture that was accompanied by changes in karyotype patterns and slightly more limited growth rate com- pared to haploid and diploid cells. Stress stimuli did not potentiate TE activity. Elevation in chromosomal DNA breaks was also observed during long-term culture of cells of different ploidy, however this was not correlated with increased TE activity. Our results suggest that increased TE activity may promote genomic diversity and plasticity, and cellular hetero- geneity during long-term culture of C. albicans cells. In summary, an adaptive response during long-term culture of C. albicans cells of various ploidy states has been documented that is based on increased TE activity and changes in karyotype patterns. Long-term culture promoted chromosomal DNA breaks, how- ever, genetic instability did not affect cell viability. Stress conditions (fluconazole, hydrogen peroxide and hypochlorite treatments) have less pronounced effect on TE activity than culture duration (90 days). Shifts in karyotype profiles may in turn promote genomic plasticity and cellular heterogeneity that may modu- late cell fitness and lifespan and result in the selection of best adapted cells within a C. albicans cell population. OLV
Transposable element insertions in fission yeast drive adaptation to environmental stress Article in Genome Research 29(1) · December 2018 Cells are regularly exposed to a range of naturally occurring stress that can restrict growth or cause lethality. In response, cells activate expression networks with hundreds of genes that together increase resistance to common environmental insults. However, stress response networks can be insufficient to ensure survival, which raises the question of whether cells possess genetic programs that can promote adaptation to novel forms of stress. We found transposable element (TE) mobility in Schizosaccharomyces pombe was greatly increased when cells were exposed to unusual forms of stress such as heavy metals, caffeine, and the plasticizer phthalate. By subjecting TE-tagged cells to CoCl2, we found the TE integration provided the major path to resistance. Groups of insertions that provided resistance were linked to TOR regulation and metal response genes. We extended our study of adaptation by analyzing TE positions in 57 genetically distinct wild strains. The genomic positions of 1048 polymorphic LTRs were strongly associated with a range of stress response genes, indicating TE integration promotes adaptation in natural conditions. These data provide strong support for the idea, first proposed by Barbara McClintock, that TEs provide a system to modify the genome in response to stress. OLV
As more discoveries get published, newer questions are raised. This undeniable fact is making biology the major branch of science where research topics multiply. We’ve heard about the issues physicists are dealing with in order to find beneficially interesting research themes that make sense. Not in biology. What we need is more funding and more students pursuing biology-related careers. This is beyond fascinating. Biology is the science area where complex functionally specified information is clearly observed. This points to conscious purpose-driven design agent, because empirically there’s no other known source for such type of information. Some papers present this situation more clearly: “many complex biological systems have a multilayer networked structure and extremely complicated nonlinear processes.” Control of multilayer biological networks and applied to target identification of complex diseases Wei Zheng, Dingjie Wang and Xiufen ZouEmail author BMC Bioinformatics201920:271 https://doi.org/10.1186/s12859-019-2841-2© The Author(s). 2019 Received: 1 April 2019Accepted: 22 April 2019Published: 28 May 2019 OLV
Question: does this research imply that conventional mutation rates could have been mis-estimated, due to measuring the mutations being measured after these clusters have done their thing? EDTA
This discovery doesn't help Darwinism one bit. Without looking at this in depth, it appears that, as BB says above, these "clusters" are formed via mutations: that is, we're dealing almost with 'clones' in various parts of an organism's body. The problem this presents is this: this 'clustering' is an overlay of mutations over any other set of mutations that took place via meiosis and fertilization (thus, inheritable mutations) with these "clustered" mutations easily becoming THE dominant mutations within these "clustered" genomes. IOW, from one generation to another, perhaps as many as 200 mutations will occur; but, that happens over 3 billion plus nucleotides with each such mutation having a very low probability of being "active" in any specialized portion of an animal's body: that is, once differentiation takes place, not all of the genome is operative in the various specialized portions of the organism and the already low odds of the inherited mutation occurring in any specialized cells now becomes even lower. IOW, the portion of the genome where one such mutation has occurred could easily be 'turned-off' in specialized cells. Now, a particular mutation, or set of mutations, has come to dominate these specialized cells and because this/these mutation(s) have occurred post-fertilization, this is much more like an epigenetic effect. So, here's where the problem(s) come in: the 'phenotype' of the organism has now become dissociated (to some degree) with its 'genotype.' How, then, does "survival of the fittest" get transmitted when the mutations have occurred "downstream", if you will? Further, this also suggests that NS will be most powerful when the animal is young--that is, "before" the "clonal" mutations ('clusters') begin to form. Yet, when animals are 'young,' they are most susceptible to random effects of the environment. Thus 'beneficial' mutations (which can be transmitted to future generations) are really not operative. What's more at play is just simple 'luck.' Now, it's hard to gauge the degree to which this is true; nevertheless, this represents a dilution of the NS + RV view evolutionists employ. PaV
Remember the Selfish Gene? Aw, he was just playin’ you guys. You didn’t fall for that, did you?
What does this have to do with the “selfish gene”? This paper just demonstrated that some body tissues are more prone to mutation than others. Skin, lungs, throat, which is not surprising as these are the least protected from environmental influences. Brother Brian

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