Fertilization marks the beginning of new life in sexually reproducing organisms. Importantly, this moment when two haploid gametes (e.g. egg and sperm cells) fuse is also the time when the newly formed diploid cell switches fate and becomes a zygote. Gamete-to-zygote fate switch is, on one hand, important to stop further mating and refertilization, and thus prevent abnormal ploidy. On the other hand, zygotic fate acquisition is crucial to initiate development, which is best evident in animal species where terminally differentiated egg and sperm cells fuse to gives rise to a totipotent zygote capable of developing into a new individual. What are the molecular mechanisms that drive the gamete-to-zygote transition has been difficult to study in animal species, where gametes and zygotes are often poorly accessible and with limited genetic tools. We previously showed striking similarities between zygotes of fission yeast and higher eukaryotes and in this ERC-funded project use this powerful model to explore molecular mechanisms that regulate zygotic fate establishment and subsequent development.
Specifically, our work has the following two aims:
1. Defining the regulation of zygotic gene expression, signalling and mechanisms that prevent refertilization. In this study, we aim to fill the knowledge gap concerning how both transcriptional and post-transcriptional regulation contribute to the development of zygotes. On one hand, we will aim to identify key molecular player and the pathways they regulate in zygotes. On the other hand, by looking and multiple pathways we aim to uncover how these regulatory modules come together and thus understand how a single decision to switch fate leads to coordinated changes in different aspects of cellular physiology, helping us grasp the principles of cell fate switching. Additionally, we will explore how fungi prevent re-fertilization, a critical aspect that is currently very poorly understood. By dissecting the molecular mechanisms behind fungal re-fertilization blocks, we may identify conserved mechanisms that are relevant to sexual reproduction in other phyla. Furthermore, studying re-fertilization blocks in a microbial context may unveil unexpected adaptive roles, as polyploidy resulting from re-fertilization can enhance fitness under specific conditions in both non-pathogenic and pathogenic species.
2. Characterizing the prevalence, roles and regulation of parent-biased allele expression. This work pushes beyond our discovery that fission yeast asymmetrically rely on parental alleles, which underlies several phenomena of non-Mendelian inheritance in higher eukaryotes. Multiple theoretical frameworks propose mechanisms for their selective evolution and yet, little experimental evidence is available since means to manipulate current model systems are limited. By identifying novel examples and roles for parent-biased allelic expression, we may introduce fission yeast as a model system, where experimental evolution is feasible, to study parent-biased gene expression. Thus, our work holds potential for major impact on understanding the evolutionary pressures that shape asymmetry in contributions of parental genomes in other phyla.
