Working Paper Hypothesis Version 1 This version is not peer-reviewed

Unveiling Human Non-random Genome Editing Mechanisms Activated in Response to Chronic Environmental Changes. I. Where Might These Mechanisms Come From?

Version 1 : Received: 17 July 2020 / Approved: 19 July 2020 / Online: 19 July 2020 (19:35:46 CEST)

How to cite: Zamai, L. Unveiling Human Non-random Genome Editing Mechanisms Activated in Response to Chronic Environmental Changes. I. Where Might These Mechanisms Come From?. Preprints 2020, 2020070427 Zamai, L. Unveiling Human Non-random Genome Editing Mechanisms Activated in Response to Chronic Environmental Changes. I. Where Might These Mechanisms Come From?. Preprints 2020, 2020070427

Abstract

This article challenges the notion of the randomness of mutations in eukaryotic cells by unveiling stress-induced human non-random genome editing mechanisms. To account for the existence of such mechanisms, I have developed molecular concepts of the cell environment and cell environmental stressors and, making use of a large quantity of published data, hypothesized the origin of some crucial biological leaps along the evolutionary path of life on Earth under the pressure of natural selection, in particular, 1) virus-cell mating as a primordial form of sexual recombination and symbiosis; 2) Lamarckian CRISPR-Cas systems; 3) eukaryotic gene development; 4) antiviral activity of retrotransposon-guided mutagenic enzymes and finally; 5) the exaptation of antiviral mutagenic mechanisms to stress-induced genome editing mechanisms directed at “hypertranscribed” endogenous genes. Genes transcribed at their maximum rate (hypertranscribed), yet still unable to meet new chronic environmental demands generated by “pollution”, are inadequate and generate more and more intronic retrotransposon transcripts. In this scenario, RNA-guided mutagenic enzymes (e.g. AID/APOBECs), which have been shown to bind to retrotransposon RNA-repetitive sequences, would be surgically targeted by intronic retrotransposons on opened chromatin regions of the same “hypertranscribed” genes. RNA-guided mutagenic enzymes may therefore “Lamarkianly” generate single nucleotide polymorphisms (SNP) and copy number variations (CNV), as well as transposon transposition and chromosomal translocations in the restricted areas of hyperfunctional and inadequate genes, leaving intact the rest of the genome. CNV and SNP of hypertranscribed genes may allow cells to surgically explore a new fitness scenario, which increases their adaptability to stressful environmental conditions. Like the mechanisms of immunoglobulin somatic hypermutation, non-random genome editing mechanisms may generate several cell mutants, and those codifying for the most environmentally-adequate proteins would have a survival advantage and would therefore be Darwinianly selected. Non-random genome editing mechanisms represent a link between environmental changes and biological novelty and plasticity, and provide a molecular basis to reconcile gene-centered and “ecological” views of evolution.

Subject Areas

environment; virus; pollutant; evolution; exaptation; stem cells; transposons; APOBEC; ADAR,; ORF2p; cancer; Eco-Evo-Devo; symbiosis; ecological genomics; environmental stress; genetic recombination; biological plasticity; hypermutation; epigenetics; fractal systems; natural selection

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