Title

RNA Splicing Cofactor Effect on FBF Protein Function in C. elegans

Presentation Type

Presentation

Abstract

The FBF proteins (FBF-1 and FBF-2) are critical to stem cell maintenance in the nematode, Caenorhabditis elegans. The hermaphroditic C. elegans initially produce sperm, and then continue with oogenesis. The FBF proteins function by regulating the transition between mitosis and meiosis by suppressing translation of specific mRNAs into proteins. FBF-1 and FBF-2 also regulate the sperm to oocyte switch in the hermaphrodite, and when FBF protein function is disrupted, there is complete sterility in the nematode. The objective of this research is to determine if certain components of pre mRNA splicing machinery have an effect on FBF protein function. For this research, an RNAi assay was used to disrupt the splicing factor function, and determine the effect of this disruption on FBF function in mutant or control worms. In two mutant strains, either FBF-1 or FBF-2 were functioning in isolation, and the control worms had both FBF-1 and FBF-2 functioning normally. The strains were synchronized by bleaching, and placed on RNAi plates containing bacteria that had been transformed to target the splicing factors of interest. The C. elegans were allowed to grow to adulthood and then the number of fertile adults were counted and recorded. Of the six total splicing factors studied, three of the knock-downs show a possible effect on FBF-2 protein function when it doesn’t have FBF-1 as a backup, two have little to no effect and one produces complete sterility in all strains. This research uncovers what could be an exciting link between RNA splicing in the nucleus and regulated protein production in the cytoplasm necessary for stem cell maintenance.

Category

Life Sciences

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Apr 17th, 2:00 PM Apr 17th, 2:20 PM

RNA Splicing Cofactor Effect on FBF Protein Function in C. elegans

UC 332

The FBF proteins (FBF-1 and FBF-2) are critical to stem cell maintenance in the nematode, Caenorhabditis elegans. The hermaphroditic C. elegans initially produce sperm, and then continue with oogenesis. The FBF proteins function by regulating the transition between mitosis and meiosis by suppressing translation of specific mRNAs into proteins. FBF-1 and FBF-2 also regulate the sperm to oocyte switch in the hermaphrodite, and when FBF protein function is disrupted, there is complete sterility in the nematode. The objective of this research is to determine if certain components of pre mRNA splicing machinery have an effect on FBF protein function. For this research, an RNAi assay was used to disrupt the splicing factor function, and determine the effect of this disruption on FBF function in mutant or control worms. In two mutant strains, either FBF-1 or FBF-2 were functioning in isolation, and the control worms had both FBF-1 and FBF-2 functioning normally. The strains were synchronized by bleaching, and placed on RNAi plates containing bacteria that had been transformed to target the splicing factors of interest. The C. elegans were allowed to grow to adulthood and then the number of fertile adults were counted and recorded. Of the six total splicing factors studied, three of the knock-downs show a possible effect on FBF-2 protein function when it doesn’t have FBF-1 as a backup, two have little to no effect and one produces complete sterility in all strains. This research uncovers what could be an exciting link between RNA splicing in the nucleus and regulated protein production in the cytoplasm necessary for stem cell maintenance.