Approximately 45% of the human genome is comprised of TEs. TEs are not simply "junk" DNA. The effects of TE insertion in the genome varies from negligible to disease conditions suh as cancer. On the other hand;TEs activity can play an essential role in the host response to stress, facilitating the adaptation of populations and species facing changing environments. Enhanced TE mobility has to be sufficient for generating broad genetic variation within the host genome, and that this genetic variability is genetically transmissible to the next generations.
I agree with Sezer, and read the last paper. The use of adaptation is referring to the cancer cells adaptation for survival, not the host organisms survival. Transposable elements, when placed in a favorable spot in the genome, can provide a beneficial effect to the genome thus providing an adaptation. In your case, a transposable element that has been activated in a cancer cell can "jump" and alter gene expression leading to an adaptation for the cancer cell's survival.
The complexity of cancer biology cannot explained by somatic mutation and clonal selection.
"Adult organisms have to adapt to survive, and the same is true for their tissues. Rates and types of cell production must be rapidly and reversibly adjusted to meet tissue demands in response to both local and systemic challenges. Recent work reveals how stem cell populations meet these requirements by switching between functional states tuned to homoeostasis or regeneration. This plasticity extends to differentiating cells, which are capable of reverting to stem cells after injury.
A substantial body of evidence supports the conclusion that chronic inflammation can predispose an individual to cancer, as demonstrated by the association between chronic inflammatory bowel diseases and the increased risk of colon carcinoma. Chronic inflammation is caused by a variety of factors, including bacterial, viral, and etc. The longer the inflammation persists, the higher the risk of associated carcinogenesis. Inflammatory mediators contribute to neoplasia by inducing stem cell adaptive responses"
Cancer is an adaptation mechanism of the aged stem cell against stress.Tez M. Rejuvenation Res. 2008 Dec;11(6):1059-60. doi: 10.1089/rej.2008.0797.
Switching roles: the functional plasticity of adult tissue stem cells.
Wabik A, Jones PH.
EMBO J. 2015 Mar 26. pii: e201490386.
Chronic inflammation and cancer: the role of the mitochondria.
Kamp DW, Shacter E, Weitzman SA
.Oncology (Williston Park). 2011 Apr 30;25(5):400-10, 413.
If Its getting mobilized in germ cells then passes to next generation, and host system also evolves during developmental processes but TEs and new lncRNAs evolves faster than genes, this makes the example of negative frequency dependent selection. I think that it may or may not be adapted for host cells
for example the new germ line integrations of L1 elements in various cancers, they also regulate the host gene or neighbor genes where they integrate.
Yes, that would explain that whether that particular locus is under selection or not.
In addition to this, new insertions may also act as bidirectional promoters, where there can drive gene expression on either of directions
Dear Friends
Thanks for your valuable contributions.
Dear Rick
I think transposable elements are switch of adaptation engine.
Cancer is an chaotic behaviour of the cell; on the other hand chaos is the best behaviour (it is true for animal cell, plant cell, economy etc.) of adaptation in the unknown milieu. Please think carcinogenesis from this respect.
Best regards
mesut
There is a cost to some individuals, in the form of congenital defects, or cancers in later life (usually in old age) attributable to TE activity or presence. However, for the lineage as a whole transposable elements generate realisable adaptive potential and realisable evolutionary potential i.e. they can result in adaptation, or in evolution, or both of these. According to the TE-thrust hypothesis (Oliver and Greene 2011, 2012, 2013) Transposable Elements are powerful facilitators of both adaptation and evolution.
I add that a loss of viable TEs may ultimately result in 'living fossils' or the extinction of the lineage
Mesut,
A very good question.
The TE can change the genome topology.
The detailed linkage with cancer has been discussed by Adam Wilkins a few years ago.
The enemy within: an epigenetic role of retrotransposons in cancer initiation.
Wilkins AS.
Bioessays. 2010 Oct;32(10):856-65.
Henry
http://www.ncbi.nlm.nih.gov/pubmed/20715060
Chalopin et al. 2013 appear to have implied that data on Transposable Elements in the coelacanth are in conflict with the TE-Thrust hypothesis, but there is no conflict. They found a small (~25% of the genome compared to ~45% for humans) of extremely large diversity TE superfamilies, and families which exhibited little recent activity. In Oliver & Greene 2011, a small highly diverse, but largely non-viable, TE population in a lineage is predicted to result in stasis, with minimal TE-Thrust. where is the conflict?
Oliver KR & Greene WG Mobile DNA and the TE-Thrust Hypothesis: Supporting evidence from the primates. Mobile DNA 2011 2:8
For the last 5 years, I have been investigating the role of transposable elements in cancer. Currently, I'm not sure they represent a relevant force involved in cancer origin and/or cancer development. Most somatic integration events take place into late replicating / not expressed regions of the genome. There is still too many quesiton marks open. See Science 08/2014; 345(6196):1251343. DOI:10.1126/science.1251343
i disagree strongly with the following assertion:
"On the other hand;TEs activity can play an essential role in the host response to stress, facilitating the adaptation of populations and species facing changing environments.
Do transposable elements (TEs) indicate that cancer is an adaptation mechanism?. "
There is no evidence whatsoever that TE activity plays any positive role in host response to stress—nor do arguments at the level of species and populations carry much weight. No, cancer is not an "adaptation mechanism".
i humbly suggest you read and re-read chapter 7on transposable elements of Genes in Conflict: The Biology of Selfish Genetic Elements, A. Burt and R. Trivers 2006. Harvard University Press. As for cancer, glance at chapter 11 for a few words.
Dear Trivers
It is not easy to say " cancer is not an adaptation mechanism".
First events in cancer remain elusive. This is not surprising: the initiating events in cancer are comparatively rare and do not produce an obviously aberrant cellular phenotype. The statement by Nowell"The fundamental nature of carcinogenesis, and degree to which it is specific for each neoplasm, remains a basic problem in cancer research". in his classic 1976 review, remains pertinent today.
best regards
In reply to Robert Trivers.
Dear Robert,
With respect, the "assertion" is not an assertion but is a hypothesis, a provisional statement with much supporting evidence, that is put up for testing. You can read it in full in the TE-Thrust hypothesis. I am not too worried about what Burt and Trivers said in 2007, as we have learnt a lot since then. However, I will look it up.
With regard to cancer, an extremely complex problem, I suspect that some TEs can cause some cancers, mostly in people past reproductive years, but their benefits in adaptation and evolution far outweigh such costs, in terms of evolution. Almost 50% of mammalian genomes are TEs (including ERVs), and it is up to 80% in some angiosperms. If it is all "selfish DNA" or "junk DNA" then natural selection must be slipping. Many biologists now see value in TEs and have good data to back these concepts. Calling it junk is going back to the 1980s, or even further back,
Keith
"but their benefits in adaptation and evolution far outweigh such costs, in terms of evolution"
this is nonsense; why don't you go back to Burt and Trivers 2006 because at least you will be up-to-date through then
"Many biologists now see value in TEs and have good data to back these concepts. Calling it junk is going back to the 1980s, or even further back,"
again, nonsense, you can not cite the "many biologists" and 2006 is not 1980; now is "natural selection slipping"—selection works at the individual level and at the genie level and it is well known that selection at the latter level can easily overwhelm selection at the individual level
but remain ignorant if that helps you in your life; re read 6000 papers and included 1500 in our bibliography; the book was reviewed as the greatest or one of the greatest books on evolutionary genetics in 50 years—hey but why pay attention to reality when you can just state long-outdated foolishness
Yes i agree, TEs must surely cause cancers at a regular rate every generation; they can generate the initial cancerous cell and modify its traits on the way. Natural selection is not absent, it occurs within cancers usually for the most proliferative variants
Hi Robert Trivers,
I own a copy of your book. I will do a deal with you - I will read the Chapters you suggest with an open mind, if you do likewise with the papers by Oliver & Greene & Oliver et al. and for good measure read Lynch et al. 2015 'Ancient Transposable Elements Transformed the Uterine Regulatory Landscape and Transcriptome during the Evolution of Mammalian Pregnancy' and similar papers to get another angle on the subject of TEs and evolution, and also on TEs and cancer. We can then resume this interesting discussion. Other interested people on Research Gate are invited to do the same,
Regards,
Keith
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