Horizontal Gene Transfers with or without Cell Fusions in All Categories of the Living Matter

Abstract

This article reviews the history of widespread exchanges of genetic segments initiated over 3 billion years ago, to be part of their life style, by sphero-protoplastic cells, the ancestors of archaea, prokaryota, and eukaryota. These primordial cells shared a hostile anaerobic and overheated environment and competed for survival. "Coexist with, or subdue and conquer, expropriate its most useful possessions, or symbiose with it, your competitor" remain cellular life's basic rules. This author emphasizes the role of viruses, both in mediating cell fusions, such as the formation of the first eukaryotic cell(s) from a united crenarchaeon and prokaryota, and the transfer of host cell genes integrated into viral (phages) genomes. After rising above the Darwinian threshold, rigid rules of speciation and vertical inheritance in the three domains of life were established, but horizontal gene transfers with or without cell fusions were never abolished. The author proves with extensive, yet highly selective documentation, that not only unicellular microorganisms, but the most complex multicellular entities of the highest ranks resort to, and practice, cell fusions, and donate and accept horizontally (laterally) transferred genes. Cell fusions and horizontally exchanged genetic materials remain the fundamental attributes and inherent characteristics of the living matter, whether occurring accidentally or sought after intentionally. These events occur to cells stagnating for some 3 milliard years at a lower yet amazingly sophisticated level of evolution, and to cells achieving the highest degree of differentiation, and thus functioning in dependence on the support of a most advanced multicellular host, like those of the human brain. No living cell is completely exempt from gene drains or gene insertions.

Molecular biology of oncogenic inflammatory processes. I. Non-oncogenic and oncogenic pathogens, intrinsic inflammatory reactions without pathogens, and microRNA/DNA interactions (Review)

“…While the omnipresent cytoplasmic filamentous structures were not unenveloped myxo, or retroviral strands (587ab,588), but products of the endoplasmic reticulum in response to IFNαβ oversecretion, serological and biochemical evidence for a herpesvirus (EBV) triggering the maturation of endogenous retrovirus(es) is becoming steadily more convincing throughout of the passing decades (62,152,474).…”

“…The advanced B7 systems are nonexistent in teleost and bony fish that are in possession of the VDJ/RAG/RSS (variable, diversity, joining; recombination activating genes; recombination signal sequences) systems. The advanced B7 and ICOS (inducible T cell costimulator) systems were acquired later in the evolutionary scale (61,62).…”

“…+ diffuse large B cell lymphoma in the elderly; it is associated with brain lymphomas in patients with AIDS, it is present in multifocal pediatric leiomyosarcomas, and in gastric carcinomas in Japan (reviewed in refs. 62,443). In autoimmune diseases (lupus erythematosus, multiple sclerosis), there is an interaction between EBV and latent endogenous retrovirus(es).…”

“…In autoimmune diseases (lupus erythematosus, multiple sclerosis), there is an interaction between EBV and latent endogenous retrovirus(es). Herpesviruses trigger the maturation of latent endogenous retroviruses, which appear budding from lymphoid cells, ReedSternberg cells, and even the transformed lymphoendothelial cells of Kaposi's sarcoma (62,108,178,464).…”

“…Its pathogenesis generated an excessive literature that was recently and repeatedly reviewed in ref. 62. In a brief summary for a very complex issue (by a clinical oncologisthematologistinfectious diseases specialist, who has had the opportunity to diagnose and treat patients with H. pyloriinduced MALT lymphomas): CagA entering lymphocytes and/or gastric mucosal epithelial cells, undergoes phosphorylation, binds Src kinase and src homology domain 2containing tyrosine phosphatase (Rous sarcoma csrc protooncogene) and activates extracellular signalregulated kinase (ERK).…”