Understanding the origin of parthenogenesis

University Of Missouri-Columbia, Columbia MO

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Abstract

Project Summary Parthenogenesis (i.e., reproduction without mating) has evolved from sexual reproduction in nearly all major eukaryotic groups. In parthenogenesis, chromosomally unreduced (e.g., diploid) gametes result from modified forms of meiosis. Understanding the genetic mechanisms underlying the modification of meiosis in parthenogenetic lineages is of significant public health interest because meiosis is central to sexual reproduction. Using parthenogenesis to understand the genetic regulation of meiosis is also a highly innovative approach, with its natural history perspective most likely yielding novel knowledge about meiosis. Using a combination of evolutionary and functional genomic approaches, this project examines the genetic bases of cyclical and obligate parthenogenesis in the freshwater microcrustacean Daphnia. Daphnia is well known for its cyclical parthenogenesis (CP) life cycle, i.e., propagating asexually under favorable environmental conditions and switching to sexual reproduction in response to stressful environment. Interestingly, some populations of the species D. pulex (backcrosses of two parental CP species D. pulex and D. pulicaria) reproduce by obligate parthenogenesis (OP) because they lost the capability to engage in sex. My lab has two long-term goals. First, considering that environmental conditions can trigger CP Daphnia to switch between parthenogenetic and sexual reproduction, environment-mediated gene expression changes most likely play the role of master regulator for reproductive mode. Our recent transcriptomic analyses revealed the many paralogous genes in the Daphnia genome show divergent expression associated with reproduction mode. For example, one paralog is upregulated in parthenogenesis, whereas the other paralog is upregulated in sexual reproduction. These paralogous contain multiple transmembrane receptors, neurotransmitter receptors, and transcription factors. We therefore hypothesize that these paralogs contain the master regulator of cyclical parthenogenesis. To identify the master regulator(s), we plan to use forward genetic screening to identify mutants that are not able to switch reproductive modes and identify the causal genes using functional analysis such as CRISPR gene editing. We will also directly perform gene knockout experiments to examine the functions of the divergently expressed paralogs in relation to reproduction in CP Daphnia. Second, concerning the origin of OP, we hypothesize that incompatible genetic elements between the two parental species CP D. pulex and CP D. pulicaria are responsible for the loss of sexual reproduction. To identify the causal incompatible elements, our lab will perform large-scale association mapping on newly discovered D. pulex crosses (between CP D. pulex isolate carrying D. pulicaria introgression) that produce both OP and CP F1s. The identified candidates will undergo functional genomics analysis (e.g., CRISPR gene knock-out), with the goal of re-creating OP animals by introducing OP-causal elements to CP Daphnia using gene editing. Lastly, we will examine whether the identified elements are present in natural OP isolates to understand whether multiple genetic mechanisms underlie the origin of OP.