Analysis of alin-42/periodNull Allele Implicates All Three Isoforms in Regulation ofCaenorhabditis elegansMolting and Developmental Timing
Autor: | Theresa L. Edelman, Ann E. Rougvie, Angela Barr, Erik M. Jorgensen, Katherine A McCulloch, Christian Frøkjær-Jensen |
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Rok vydání: | 2016 |
Předmět: |
0301 basic medicine
Gene isoform Genotype Transcription Genetic Penetrance Locus (genetics) QH426-470 Investigations Animals Genetically Modified 03 medical and health sciences 0302 clinical medicine heterochrony Genetics Animals Protein Isoforms Allele Caenorhabditis elegans Caenorhabditis elegans Proteins Molecular Biology Gene lin-42 Alleles Genetics (clinical) biology molting fungi Gene Expression Regulation Developmental biology.organism_classification Null allele Phenotype 030104 developmental biology Genetic Loci Heterochrony 030217 neurology & neurosurgery Transcription Factors |
Zdroj: | G3: Genes|Genomes|Genetics G3: Genes, Genomes, Genetics, Vol 6, Iss 12, Pp 4077-4086 (2016) |
ISSN: | 2160-1836 |
DOI: | 10.1534/g3.116.034165 |
Popis: | 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. |
Databáze: | OpenAIRE |
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