Drosophila melanogaster tissues carrying a third chromosome with the deletion Df(3R)karD2 make a 40,000-dalton (Dal) heat shock protein not made by wild type. The unusual polypeptide was inducible in every tissue examined. Tryptic peptide fingerprints showed it to include part of the 70,000-Dal major heat shock protein. Mapping experiments placed the mutation responsible for the 40,000-Dal protein at or close to the karD2 deletion. One break point of the deletion is in subdivision 87A, close to or at a heat shock locus that codes for the 70,000-Dal protein. The results are consistent with the possibility that this break point is within a gene for the 70,000-Dal protein, leaving only the initial portion of its coding sequence. This would specify the direction of transcription of the mutant gene as proximal to distal on the normal chromosome. The 87A heat shock locus should contain at least two genes for the 70,000-Dal protein, because embryos homozygous for the karD2 deletion and lacking the heat shock locus at 87C, which also codes for the 70,000-Dal protein, nevertheless produced both the 40,000-Dal and the 70,000-Dal proteins upon temperature elevation. Using the presence of the 40,000-Dal protein to monitor chromosome segregation, we found that embryos homozygous for deletions of the heat shock puff site at 93D exhibited a normal electrophoretic pattern of heat shock proteins.Heat shock (HS) and certain other treatments induce puffs at specific sites on the polytene chromosomes of Drosophila (1-3) and induce the synthesis of specific polypeptides (4-6). The response is not tissue specific (7) and occurs also in cultured cells (6). From induced cultured cells, messenger RNAs have been purified that hybridize in situ at the heat shock puff sites (6,(8)(9)(10). The presence of DNA sequences coding for the major heat shock polypeptide [70,000 daltons (Dal)] at both regions 87A and 87C is indicated by the finding that messenger RNA that codes for the 70,000-Dal polypeptide in a cell-free system (11, 12) cosediments with RNA that hybridizes to both regions (11). This conclusion has been verified by showing that cloned DNA fragments that hybridize at 87A and 87C also hybridize to messenger RNA for the 70,000-Dal polypeptide (13,14). Such localization is also supported by the observation that embryos homozygous for deletions of both 87A and 87C fail to produce the 70,000-Dal polypeptide (15). Both 87A and 87C appear to contain multiple copies for the genes for the 70,000-Dal HS polypeptide (16).We report here a mutation that leads to the induction after HS of an unusual polypeptide whose sequence is part of the major HS polypeptide. The mutation maps at region 87A and appears to result from a deletion that removes part of a gene for the 70,000-Dal HS protein. The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U. S. C. §1734 solely to indicate this fact.
MATERIALS AND METHODS