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PAM1 and autophagy pathways intersect to regulate gametogenesis in Caenorhabditis elegans
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Chris Trzepacz, PhD
Presentation Format
Poster Presentation
Abstract/Description
Autophagy, the cell’s recycling system, is a highly conserved and regulated biological process. Autophagy is utilized to remove any damaged, malfunctioning, or unnecessary organelles, but can be stimulated in times of cellular stress, such as starvation or the accumulation of cytotoxic aggregates, such as those linked to neurodegenerative disorders such as Huntington’s and Alzheimer’s disease. Studies in a number of model organisms, including mice, fruit flies, and nematodes have identified numerous genes involved in mediating autophagy, including the puromycin-sensitive aminopeptidase (Psa). The Caenorhabditis elegans orthologue of Psa, pam-1, also governs fertility. We have examined the involvement of autophagy in gametogenesis. RNAi was employed to independently inhibit the expression of five conserved C. elegans autophagy genes and adult animals were examined for changes in pam-1-influenced phenotype metrics: brood size, embryonic fertility, expansion of immature, pachytene stage germinal nuclei in the gonads, and oocyte nucleolar disassembly. RNAi of the autophagy genes has minimal impact on the N2 animals. However, the independent inhibition of each of the autophagy genes in mutant pam1 animals results in a synergistic exacerbation of multiple fertility metrics, most consistently an expansion of the pachytene population. We are currently employing transgenic animals to verify the intersection of PAM-1 and autophagy functions in mediating meiotic transitions and fertility in C. elegans.
Location
Large Ballroom, Curris Center
Start Date
April 2016
End Date
April 2016
PAM1 and autophagy pathways intersect to regulate gametogenesis in Caenorhabditis elegans
Large Ballroom, Curris Center
Autophagy, the cell’s recycling system, is a highly conserved and regulated biological process. Autophagy is utilized to remove any damaged, malfunctioning, or unnecessary organelles, but can be stimulated in times of cellular stress, such as starvation or the accumulation of cytotoxic aggregates, such as those linked to neurodegenerative disorders such as Huntington’s and Alzheimer’s disease. Studies in a number of model organisms, including mice, fruit flies, and nematodes have identified numerous genes involved in mediating autophagy, including the puromycin-sensitive aminopeptidase (Psa). The Caenorhabditis elegans orthologue of Psa, pam-1, also governs fertility. We have examined the involvement of autophagy in gametogenesis. RNAi was employed to independently inhibit the expression of five conserved C. elegans autophagy genes and adult animals were examined for changes in pam-1-influenced phenotype metrics: brood size, embryonic fertility, expansion of immature, pachytene stage germinal nuclei in the gonads, and oocyte nucleolar disassembly. RNAi of the autophagy genes has minimal impact on the N2 animals. However, the independent inhibition of each of the autophagy genes in mutant pam1 animals results in a synergistic exacerbation of multiple fertility metrics, most consistently an expansion of the pachytene population. We are currently employing transgenic animals to verify the intersection of PAM-1 and autophagy functions in mediating meiotic transitions and fertility in C. elegans.