Photoperiodic induction of diapause requires regulated transcription of timeless in the larval brain of Chymomyza costata
Language English Country United States Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
18375862
DOI
10.1177/0748730407313364
PII: 23/2/129
Knihovny.cz E-resources
- MeSH
- Biological Clocks physiology MeSH
- Circadian Rhythm physiology MeSH
- Drosophilidae physiology MeSH
- Photoperiod * MeSH
- Transcription, Genetic * MeSH
- Insect Proteins genetics metabolism MeSH
- Larva cytology metabolism MeSH
- RNA, Messenger metabolism MeSH
- Life Cycle Stages * MeSH
- Animals MeSH
- Check Tag
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Insect Proteins MeSH
- RNA, Messenger MeSH
Photoperiodic signal stimulates induction of larval diapause in Chymomyza costata. Larvae of NPD strain (npd-mutants) do not respond to photoperiod. Our previous results indicated that the locus npd could code for the timeless gene and its product might represent a molecular link between circadian and photoperiodic clock systems. Here we present results of tim mRNA (real time-PCR) and TIM protein (immunohistochemistry) analyses in the larval brain. TIM protein was localized in 2 neurons of each brain hemisphere of the 4-d-old 3rd instar wild-type larvae. In a marked contrast, no TIM neurons were detected in the brain of 4-day-old 3rd instar npd -mutant larvae and the level of tim transcripts was approximately 10-fold lower in the NPD than in the wild-type strain. Daily changes in tim expression and TIM presence appeared to be under photoperiodic control in the wild-type larvae. Clear daily oscillations of tim transcription were observed during the development of 3rd instars under the short-day conditions. Daily oscillations were less apparent under the long-day conditions, where a gradual increase of tim transcript abundance appeared as a prevailing trend. Analysis of the genomic structure of tim gene revealed that npd-mutants carry a 1855 bp-long deletion in the 5'-UTR region. This deletion removed the start of transcription and promoter regulatory motifs E-box and TER-box. The authors hypothesize that this mutation was responsible for dramatic reduction of tim transcription rates, disruption of circadian clock function, and disruption of photoperiodic calendar function in npd-mutant larvae of C. costata.
References provided by Crossref.org
Coevolution of Drosophila-type timeless with partner clock proteins
