The 21-nucleotide let-7 RNA regulates developmental timing in Caenorhabditis elegans

Nature ◽  
2000 ◽  
Vol 403 (6772) ◽  
pp. 901-906 ◽  
Author(s):  
Brenda J. Reinhart ◽  
Frank J. Slack ◽  
Michael Basson ◽  
Amy E. Pasquinelli ◽  
Jill C. Bettinger ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Developmental Timing

scholarly journals Analysis of a lin-42/period Null Allele Implicates All Three Isoforms in Regulation of Caenorhabditis elegans Molting and Developmental Timing

2016 ◽  
Vol 6 (12) ◽  
pp. 4077-4086 ◽  
Author(s):  
Theresa L B Edelman ◽  
Katherine A McCulloch ◽  
Angela Barr ◽  
Christian Frøkjær-Jensen ◽  
Erik M Jorgensen ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Null Allele ◽  
Postembryonic Development ◽  
Developmental Timing ◽  
Critical Element ◽  
Coding Region ◽  
Protein Coding ◽  
Temporal Regulation ◽  
Larval Stages ◽  
Hypomorphic Alleles

Abstract The Caenorhabditis elegans heterochronic gene pathway regulates the relative timing of events during postembryonic development. lin-42, the worm homolog of the circadian clock gene, period, is a critical element of this pathway. lin-42 function has been defined by a set of hypomorphic alleles that cause precocious phenotypes, in which later developmental events, such as the terminal differentiation of hypodermal cells, occur too early. A subset of alleles also reveals a significant role for lin-42 in molting; larval stages are lengthened and ecdysis often fails in these mutant animals. lin-42 is a complex locus, encoding overlapping and nonoverlapping isoforms. Although existing alleles that affect subsets of isoforms have illuminated important and distinct roles for this gene in developmental timing, molting, and the decision to enter the alternative dauer state, it is essential to have a null allele to understand all of the roles of lin-42 and its individual isoforms. To remedy this problem and discover the null phenotype, we engineered an allele that deletes the entire lin-42 protein-coding region. lin-42 null mutants are homozygously viable, but have more severe phenotypes than observed in previously characterized hypomorphic alleles. We also provide additional evidence for this conclusion by using the null allele as a base for reintroducing different isoforms, showing that each isoform can provide heterochronic and molting pathway activities. Transcript levels of the nonoverlapping isoforms appear to be under coordinate temporal regulation, despite being driven by independent promoters. The lin-42 null allele will continue to be an important tool for dissecting the functions of lin-42 in molting and developmental timing.

scholarly journals ALG-5 is a miRNA-associated Argonaute required for proper developmental timing in the Caenorhabditis elegans germline

2017 ◽  
Vol 45 (15) ◽  
pp. 9093-9107 ◽  
Author(s):  
Kristen C. Brown ◽  
Joshua M. Svendsen ◽  
Rachel M. Tucci ◽  
Brooke E. Montgomery ◽  
Taiowa A. Montgomery
Keyword(s):  
Caenorhabditis Elegans ◽  
Developmental Timing

scholarly journals The let-7 MicroRNA Family Members mir-48, mir-84, and mir-241 Function Together to Regulate Developmental Timing in Caenorhabditis elegans

2006 ◽  
Vol 10 (2) ◽  
pp. 271 ◽  
Author(s):  
Allison L. Abbott ◽  
Ezequiel Alvarez-Saavedra ◽  
Eric A. Miska ◽  
Nelson C. Lau ◽  
David P. Bartel ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Family Members ◽  
Developmental Timing ◽  
Microrna Family

scholarly journals Caenorhabditis elegans microRNAs of the let-7 family act in innate immune response circuits and confer robust developmental timing against pathogen stress

2015 ◽  
Vol 112 (18) ◽  
pp. E2366-E2375 ◽  
Author(s):  
Zhiji Ren ◽  
Victor R. Ambros
Keyword(s):  
Immune Response ◽  
Caenorhabditis Elegans ◽  
P38 Mapk ◽  
Innate Immune Response ◽  
Regulatory Networks ◽  
Mapk Pathway ◽  
Regulation Of Gene Expression ◽  
Innate Immune ◽  
Developmental Timing ◽  
C Elegans

Animals maintain their developmental robustness against natural stresses through numerous regulatory mechanisms, including the posttranscriptional regulation of gene expression by microRNAs (miRNAs). Caenorhabditis elegans miRNAs of the let-7 family (let-7-Fam) function semiredundantly to confer robust stage specificity of cell fates in the hypodermal seam cell lineages. Here, we show reciprocal regulatory interactions between let-7-Fam miRNAs and the innate immune response pathway in C. elegans. Upon infection of C. elegans larvae with the opportunistic human pathogen Pseudomonas aeruginosa, the developmental timing defects of certain let-7-Fam miRNA mutants are enhanced. This enhancement is mediated by the p38 MAPK innate immune pathway acting in opposition to let-7-Fam miRNA activity, possibly via the downstream Activating Transcription Factor-7 (ATF-7). Furthermore, let-7-Fam miRNAs appear to exert negative regulation on the worm’s resistance to P. aeruginosa infection. Our results show that the inhibition of pathogen resistance by let-7 involves downstream heterochronic genes and the p38 MAPK pathway. These findings suggest that let-7-Fam miRNAs are integrated into innate immunity gene regulatory networks, such that this family of miRNAs modulates immune responses while also ensuring robust timing of developmental events under pathogen stress.

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