| Budget Amount *help |
¥6,500,000 (Direct Cost: ¥6,500,000)
Fiscal Year 1988: ¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1987: ¥4,500,000 (Direct Cost: ¥4,500,000)
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| Research Abstract |
In the present work, the following two lines of experiments were carried out and the abnormal optic morphologies in Bar and Om(1D) mutants of Drosophila were shown to be resulted from the insertional activation of a new, common homeobox-containing gene, Om(1D)/bar gene.
EXP.1:The tom element, putatively associated with optic morphology mutations in Drosophila ananassae was identified as a retrovirus-like transposoble element. The tom element was found to terminate with 475 base pair direct repeats which are identical in sequence to each other. Southern blot and heteroduplex analyses showed the tom element to have high homology to 297 and 17.6, two retrotransposons found in D.melanogaster. As in the cases of 297 and 17.6, tom includes the nucleotide seqeuences coding for a presumptive protease and reverse transcriptase, similar in amino acid sequence to those of the Moloney murine leukaemia virus. The insertion of tom appears to be carried out in a sequence specific fashion using ATAT as a target.
EXP.2:The genome structures of various Om(1D) alleles together with their revertants were analyzed and it was found that the activation of a newly identified, homeobox-containing Om(1D) gene by the inserted tom element to be the primary cause of Om(1D) mutations. Cytological experiments show the D.melanogaster Om(1D) gene to be located near the bar locus and duplicated in the Bar mutant. The predicted Om(1D) proteins in D.ananassae and D.melanogaster, respectively, are 603 and 542 amino acids long. Taken together, our results suggest that the Om(1D) protein may be involved in the processes for size and shape detremination of the complex eyes.
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