Program in Bioinformatics and Integrative Biology
Amino Acids, Peptides, and Proteins | Biochemistry | Genetic Phenomena | Genetics | Molecular Biology | Nucleic Acids, Nucleotides, and Nucleosides
Proper regulation of germline gene expression is essential for fertility and maintaining species integrity. In the C. elegans germline, a diverse repertoire of regulatory pathways promote the expression of endogenous germline genes and limit the expression of deleterious transcripts to maintain genome homeostasis. Here we show that the conserved TRIM-NHL protein, NHL-2, plays an essential role in the C. elegans germline, modulating germline chromatin and meiotic chromosome organization. We uncover a role for NHL-2 as a co-factor in both positively (CSR-1) and negatively (HRDE-1) acting germline 22G-small RNA pathways and the somatic nuclear RNAi pathway. Furthermore, we demonstrate that NHL-2 is a bona fide RNA binding protein and, along with RNA-seq data point to a small RNA independent role for NHL-2 in regulating transcripts at the level of RNA stability. Collectively, our data implicate NHL-2 as an essential hub of gene regulatory activity in both the germline and soma.
genetics, TRIM-NHL, proteins, NHL-2, CSR-1, HRDE-1, 22G-RNA, germline, gene expression
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The copyright holder for this preprint (which was not peer-reviewed) is the author/funder. It is made available under a CC-BY 4.0 International license.
DOI of Published Version
bioRxiv 260240; doi: https://doi.org/10.1101/260240. Link to preprint on bioRxiv service.
Boag, Peter R.; Davis, Gregory M.; Tu, Shikui; Colson, Rhys N.; Anderson, Joshua W. T.; Gunzburg, Menachem J.; Francisco, Michelle A.; Ray, Debashish; Maity, Tuhin; Wu, Monica Z.; Morris, Quaid D.; Hughes, Timothy R.; Wilce, Jacqueline A.; University of Toronto; and Weng, Zhiping, "The TRIM-NHL protein NHL-2 is a Novel Co-Factor of the CSR-1 and HRDE-1 22G-RNA Pathways" (2018). University of Massachusetts Medical School Faculty Publications. 1543.
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This work is licensed under a Creative Commons Attribution 4.0 License.