ABSTRACT
The hrsω or the 93D heat shock locus of Drosophila melanogaster, which does not code for any protein, has an important role in development since nullosomy of this locus in transheterozygotes for two overlapping deficiencies, viz., Df(3R)eGp4 (eGp4) and Df(3R)GC14 (GC14), is known to cause a high (~ 80%) mortality with the small number of escapee nullosomic flies being sterile, weak and surviving for only a few days. We now show that a majority of the hsrω-nulosomics die as embryo and that the 20% escapee embryos develop slower compared to their sibs carrying either one or two copies of the hsrω locus but after hatching survive to pupal/imago stage. Most interestingly, we further show that when one hsp83 mutant allele (hsp83e4A) is introduced in eGp4/GC14 trans-heterozygotes, practically none of the hsrω-nullosomic embryos develop beyond the 1st instar larval stage. The specificity of this interaction between hsp83 and hsrω genes was further confirmed by examining the effect of the hsp83 mutant allele on other mutations in the 93D cytogenetic region. Therefore, we conclude that the hsp83 mutation acts as a dominant enhancer of the lethality associated with nullosomy for the hsrω gene. The observed genetic interaction between these two members of the heat shock gene family during normal embryonic development of Drosophila reveals novel aspects of their biological functions.