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Enhanced Northern Blot Detection of Small RNA Species in Drosophila Melanogaster
Published on: August 21, 2014
The novel gene twenty-four defines a critical translational step in the Drosophila clock
Chunghun Lim1, Jongbin Lee, Changtaek Choi
1Department of Neurobiology and Physiology, Northwestern University, Evanston, Illinois 60208, USA.
Abstract:
Daily oscillations of gene expression underlie circadian behaviours in multicellular organisms. While attention has been focused on transcriptional and post-translational mechanisms, other post-transcriptional modes have been less clearly delineated. Here we report mutants of a novel Drosophila gene twenty-four (tyf) that show weak behavioural rhythms. Weak rhythms are accompanied by marked reductions in the levels of the clock protein Period (PER) as well as more modest effects on Timeless (TIM). Nonetheless, PER induction in pacemaker neurons can rescue tyf mutant rhythms. TYF associates with a 5'-cap-binding complex, poly(A)-binding protein (PABP), as well as per and tim transcripts. Furthermore, TYF activates reporter expression when tethered to reporter messenger RNA even in vitro. Taken together, these data indicate that TYF potently activates PER translation in pacemaker neurons to sustain robust rhythms, revealing a new and important role for translational control in the Drosophila circadian clock.
Insights
A novel gene, twenty-four (tyf), is crucial for maintaining robust circadian rhythms in Drosophila. TYF protein enhances the translation of the Period (PER) clock protein, revealing a key role for translational control in daily biological timing.
Area of Science:
- Chronobiology
- Molecular Biology
- Genetics
Background:
- Circadian rhythms are regulated by daily oscillations in gene expression.
- Transcriptional and post-translational mechanisms are well-studied, but post-transcriptional regulation remains less understood.
- The Drosophila circadian clock relies on core clock genes like Period (PER) and Timeless (TIM).
Purpose of the Study:
- To investigate the role of novel genes in regulating circadian behaviors.
- To elucidate the molecular mechanisms underlying circadian rhythm maintenance.
- To identify new regulatory elements in the Drosophila circadian clock.
Main Methods:
- Isolation and characterization of Drosophila mutants for the 'twenty-four' (tyf) gene.
- Analysis of behavioral rhythms and clock protein levels (PER, TIM).
- Biochemical assays to determine TYF protein interactions and translational activity.
Main Results:
- Mutants of the 'twenty-four' (tyf) gene exhibit weakened behavioral rhythms.
- TYF deficiency leads to reduced levels of the Period (PER) protein and, to a lesser extent, Timeless (TIM).
- TYF physically associates with PER and TIM transcripts and activates reporter gene expression, indicating a role in translation.
- Restoring PER in pacemaker neurons rescues tyf mutant rhythms.
Conclusions:
- The 'twenty-four' (tyf) gene product is essential for robust circadian rhythms in Drosophila.
- TYF acts as a potent activator of PER translation in pacemaker neurons.
- Translational control is a critical mechanism for sustaining circadian clock function.
