A non-genetic meiotic repair program inferred from spore survival values in fission yeast wild isolates: a clue for an epigenetic ratchet-like model of ageing?

Abstract

What is the nature of the ageing process? What is the spore survival, that one would expect upon analysing a self-cross, in a wild fission yeast strain? Could this two research questions be, somehow, related? In this manuscript, I am describing some interesting observations obtained while studying fission yeast spore survival values upon genetic crosses. Early findings brought my attention into mainly studying self-crosses (intra-strain crosses in which any cell can be involved in by matting with a sibling cell). This study, yield some interesting findings. As a summary: 1) most fission yeast self-crosses do show low spore survival values; 2) clonally related strains show a high phenotypic variability in self-cross spore survival values; 3) differences in self-cross spore survival values can be detected when comparing zygotic and azygotic mattings; 4) self-cross spore survival values are highly affected by environmental factors, mainly producing a reduction in the spore survival values; 5) self-cross spore survival values are "recovered" when cells are subjected to several rounds of meiotic divisions; 6) signs of correlation between spore survival and vegetative cell survival (prior to the entry into meiosis) have been observed in this study.All those observations, among others, are discussed as part of an epigenetic variability that exist in fission yeast populations. A cyclical behaviour, of this epigenetic variability it is proposed, defining an underlying ratchet-like epigenetic mechanisms acting in all cells. In

A non-Lamarckian model for the inheritance of the epigenetically-coded phenotypic characteristics: a new paradigm for Genetics, Genomics and, above all, Ageing studies

“…In this paper I would like to introduce some theoretical considerations, which, if proven right by the experimental frameworks designed to test them, might stand for a paradigmatic change on genetics, genomics and ageing studies. This paper further develops a theoretical framework previously proposed by this author (Marsellach, 2017). Despite this, this paper is written as a standalone paper, which describe in more detail the previously hinted model (Marsellach, 2017), and adds emphasis in the putative implications that, the proposed theoretical framework, might have in describing the way in which the epigenetic information is transmitted from one generation to the following ones, and in the implications that this might have for genetics, genomics and ageing studies.…”

“…As detailed later, in an ideal scenario, the Laws of Mendel should never be true for the epigenetically-coded phenotypic characteristics. This is due to the fact that there is a meiotic epigenetic repair program that should repair all the epimutations accumulated so far (see later and (Marsellach, 2017)). But the fact is that, sometimes, the Laws of Mendel, are, indeed, true for the epigenetically coded phenotypic characteristics (see below for details).…”

“…In a previous manuscript I proposed the existence of a pervasive meiotic epigenetic repair program happening in all meiotic cells. In that manuscript, it was as well hinted that: 1) the repair capacity of the cells seems to be limited (probably due to cell resources limitations), and therefore this epigenetic meiotic repair program does not always acts in all loci, and 2) there seems to be correlation between this repair capabilities and cell fitness or event lethality avoidance (so that the epigenetic defects are the main cause of cell lethality; see (Marsellach, 2017)).…”

“…On the other hand, although the association of ageing and epigenetics is not new, in recent years there has been an increasing amount of evidences that imply epigenetics as the main actor in ageing (Horvath, 2013;Zhang et al, 2015;Ocampo et al, 2016;Sen et al, 2016;Ashapkin et al, 2017;Maierhofer et al, 2017;Marsellach, 2017), even proposing epigenetics as the only cause of ageing (Gibbs, 2014;Ocampo et al, 2016;Marsellach, 2017). Nevertheless, to date there has not been any coherent explanation on how variability in the epigenome can drive ageing.…”

“…As discussed, this generates two ratchets: the well-known genetic Muller's ratchet, and the newly proposed epigenetic ratchet, which together ensure the constant production of newly-born fit individuals. See Figure 4B and (Marsellach, 2017).…”