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Mol Genet Genomics. 2011 Apr;285(4):313-23. doi: 10.1007/s00438-011-0610-7. Epub 2011 Mar 12.

Transcripts from the Drosophila heat-shock gene hsr-omega influence rates of protein synthesis but hardly affect resistance to heat knockdown.

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Centre for Environmental Stress and Adaptation Research, School of Biological Sciences, Monash University, Clayton, VIC 3800, Australia.


While hundreds of genes have recently been implicated in an organism's response to thermal stress, our insight into the cellular and physiological mechanisms affected by these genes has advanced to a lesser extent. We focus on an enigmatic Drosophila heat stress RNA gene, hsr-omega, which encodes two RNA transcripts that are constitutively expressed in almost all developing and adult tissues, omega-n in the nucleus and omega-c in the cytoplasm; both being readily induced to high levels by mild heat stress. We derived three hsr-omega mutant lines via imprecise P-element excision and characterised them for changes in expression, in both the presence and absence of heat stress. Viability estimates indicate that a low level of omega-n is required for normal development. Consistent with the model of omega-n as a negative regulator of intron-processed mRNA levels the mutants displayed a 1.5-fold increase in rates of protein synthesis measured in ovarian tissue in the absence of heat stress, a result suggesting that an important function of hsr-omega is the modulation of general protein synthesis. The mutants had little effect on two measures commonly used to assess heat tolerance, heat-knockdown time and heat hardening ability, suggesting that more subtle heat-related fitness components need to be examined for effects of these mutations.

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