The endogenous mex-3 3 UTR is required for germline repression and contributes to optimal fecundity in C. elegans
Student Authors
Mennatallah AlbarqiAcademic Program
InterdisciplinaryUMass Chan Affiliations
Biochemistry and Molecular PharmacologyMorningside Graduate School of Biomedical Sciences
Document Type
Journal ArticlePublication Date
2021-08-23Keywords
Fluorescence imagingOocytes
RNA-binding proteins
Gene expression
RNA interference
Quantitative analysis
Messenger RNA
Fecundity
Amino Acids, Peptides, and Proteins
Developmental Biology
Genetics and Genomics
Nucleic Acids, Nucleotides, and Nucleosides
Metadata
Show full item recordAbstract
RNA regulation is essential to successful reproduction. Messenger RNAs delivered from parent to progeny govern early embryonic development. RNA-binding proteins (RBPs) are the key effectors of this process, regulating the translation and stability of parental transcripts to control cell fate specification events prior to zygotic gene activation. The KH-domain RBP MEX-3 is conserved from nematode to human. It was first discovered in Caenorhabditis elegans, where it is essential for anterior cell fate and embryo viability. Here, we show that loss of the endogenous mex-3 3 UTR disrupts its germline expression pattern. An allelic series of 3 UTR deletion variants identify repressing regions of the UTR and demonstrate that repression is not precisely coupled to reproductive success. We also show that several RBPs regulate mex-3 mRNA through its 3 UTR to define its unique germline spatiotemporal expression pattern. Additionally, we find that both poly(A) tail length control and the translation initiation factor IFE-3 contribute to its expression pattern. Together, our results establish the importance of the mex-3 3 UTR to reproductive health and its expression in the germline. Our results suggest that additional mechanisms control MEX-3 function when 3 UTR regulation is compromised.Source
Albarqi MMY, Ryder SP. The endogenous mex-3 3´UTR is required for germline repression and contributes to optimal fecundity in C. elegans. PLoS Genet. 2021 Aug 23;17(8):e1009775. doi: 10.1371/journal.pgen.1009775. PMID: 34424904; PMCID: PMC8412283. Link to article on publisher's site
DOI
10.1371/journal.pgen.1009775Permanent Link to this Item
http://hdl.handle.net/20.500.14038/42105PubMed ID
34424904Related Resources
Rights
Copyright: © 2021 Albarqi, Ryder. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.Distribution License
http://creativecommons.org/licenses/by/4.0/ae974a485f413a2113503eed53cd6c53
10.1371/journal.pgen.1009775
Scopus Count
Except where otherwise noted, this item's license is described as Copyright: © 2021 Albarqi, Ryder. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.