Abstract
B chromosomes are non-essential components of numerous plant and animal genomes. Because many of these “extra” chromosomes enhance their own transmission in ways that are detrimental to the rest of the genome, they can be thought of as genome parasites. An extreme example is a paternally inherited B chromosome known as paternal sex ratio (PSR), which is found in natural populations of the jewel wasp Nasonia vitripennis. In order to ensure its own propagation, PSR severely biases the wasp sex ratio by converting diploid female-destined embryos into transmitting haploid males. This action occurs at the expense of the other paternally inherited chromosomes, which fail to resolve during the first round of division and are thus eliminated. Recent work has revealed that paternal genome elimination by PSR occurs through the disruption of a number of specific histone post-translational modifications, suggesting a central role for chromatin regulation in this phenomenon. In this review, we describe these recent advances in the light of older ones and in the context of what is currently understood about the molecular mechanisms of targeted genome silencing and elimination in other systems.
Highlights
Many heritable elements present within eukaryotic genomes – for example, protein-coding genes—arise evolutionarily and persist because they confer some level of selective advantage to the organisms in which they reside
RNA has been detected in sperm and recent work has identified a role for such RNAs in mediating transgenerational “paternal effect” phenotypes (Zhao et al, 2006; Rodgers et al, 2013). These discoveries suggest a possible route for paternal sex ratio (PSR)-transcribed gene products to be transferred via sperm into the egg where they would be able to participate in paternal genome elimination
It is speculated that prolonged and/or incomplete replication prevents chromosome resolution. It is unknown if any specific histone modifications are perturbed by Wolbachia, so no direct comparisons can be made to PSR in this regard; H4 loading occurs normally in PSR-containing embryos, as does the first round of replication (Swim et al, 2012; Aldrich et al, 2017)
Summary
Many heritable elements present within eukaryotic genomes – for example, protein-coding genes—arise evolutionarily and persist because they confer some level of selective advantage to the organisms in which they reside. PSR is unique in this regard: it is transmitted to new progeny solely via sperm and must counter its own loss by drastically altering the wasp’s sex ratio to produce all male broods This effect is initiated soon after fertilization when all of the paternal chromosomes, with the exception of PSR itself, Genome Elimination by a “Selfish” B Chromosome are eliminated as the mitotic divisions of early embryogenesis begin (Werren et al, 1981, 1987; Swim et al, 2012). Cytological studies showed that when PSR is present the paternal half of the genome becomes an abnormally compact mass (referred to as the paternal chromatin mass or PCM) that never transitions into individualized chromosomes during the first embryonic mitotic division following fertilization (Reed, 1993) (Figure 1A) This effect results in complete loss of the PCM at this earliest developmental stage. What is the molecular nature of the PCM and how are its properties different from normally functioning nuclear material? How does PSR cause PCM formation (i.e., genome elimination) at the molecular level while avoiding self-elimination? How does PSR target specific chromosomes and how is this targeting information conveyed? Here, we summarize findings from several recent studies that provide insights to these questions, emphasizing that PSR-induced genome elimination is a chromatin-based phenomenon and a prime example of conflict among elements within the same genome
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