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Kopcak, D.

Publications and source records attributed to Kopcak, D..

2 recordsLinked to original sources

A single locus carrying modified oogenesis genes underlies the switch to asexuality in Artemia brine shrimp

Transitions from sexual to asexual reproduction are well-documented across different taxa. However, despite extensive efforts, the regulatory changes underlying the emergence of asexuality remain largely undiscovered in the majority of species studied. Artemia brine shrimp have multiple closely related sexual and obligate parthenogenetic lineages, making them a promising model for addressing this question. While earlier work suggested that asexuals use a modified meiosis, and inferred a likely role for the Z-chromosome in its transmission, no master regulator or genetic changes have been put forward as the root causes for the shift. Here, we generate single-nucleus RNAseq data of the female reproductive system of individuals from the Aibi lake population of Artemia parthenogenetica and its closely related obligate sexual species Artemia sp. Kazakhstan. We identify the germline cell clusters in the female reproductive system and perform differential expression analysis to infer substantial transcriptional differences at genes putatively involved in cell cycle and oocyte development between the meiotic cells of the two species. Additionally, we use whole-genome sequencing of 32 individuals from two backcrossing experiments to narrow down the genomic regions associated with the transmission of asexuality to an 8 megabase region of the Z chromosome. Within the identified regions, two adjacent genes with known functions in oogenesis, ITPR and USP8, show differential expression and genetic differentiation between sexuals and asexuals, making them promising candidate drivers of asexuality in this species. Significance statementWhile most animals reproduce sexually, many do not, and why and how these shifts occur remains an open question. This paper presents a systematic investigation of the molecular changes that underlie the transition from sexual to asexual reproduction in brine shrimp. We combine multiple computational and experimental approaches to look for differences between close sexual and asexual lineages. We find that a subset of meiotic germ cells is regulated differently in the two, and that two important oogenesis genes are the likely drivers of asexuality. This work is unique in providing an in-depth characterization of the combined genetic and regulatory changes underlying this key transition in reproductive modes.

evolutionary biology↗

How do self-fertilising and facultative sexual populations differ in mutation accumulation?

Self-fertilisation and asexual reproduction are both hypothesised to cause long-term extinction due to inefficient selection against deleterious mutations. Self-fertilisation can counter these effects through creating homozygous genotypes and purging deleterious mutations. Although complete asexuality lacks meiotic gene exchange, mitotic gene conversion creates homozygous regions that could limit deleterious mutation accumulation in an analogous manner. We compare mutation accumulation in self-fertilising and facultative sexual populations subject to mitotic gene conversion, and quantify the efficacy of purging in the latter. We first show analytically that purging is most effective with high levels of asexuality and gene conversion, and when deleterious mutations are recessive. We further show using simulations that, when mitotic gene conversion becomes sufficiently high in obligate asexuals, there is a reduction in the mutation count and a jump in homozygosity, reflecting purging. However, this mechanism is not necessarily as efficient at purging under high self-fertilisation, and elevated rates of mitotic gene conversion seem to be needed for widespread purging compared to empirical estimates. If gene conversion rates are allowed to evolve, then elevated rates that increase mean fitness can arise, but only if there is sufficient variance in the gene conversion rate. Conversely, if gene conversion rates are already high and rates are not constrained then they will slightly decrease, reducing mean fitness. Significance StatementAsexuality has been argued to be an evolutionary dead end, due to a lack of gene exchange causing inefficient selection acting against deleterious mutations. It has been proposed that asexuals can counter these negative effects through mitotic gene conversion, which exposes mutations to selection within individual lineages. Here, we theoretically investigate how effective this mechanism is. We compare results to those obtained when individuals reproduce by self-fertilisation, which has similar effects on exposing deleterious variants. While mitotic gene conversion can be effective in removing recessive deleterious mutations, high rates are required (that are not necessarily maintained by selection) and it is not always as effective as selfing.

evolutionary biology↗