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Title: Genetic study on the effects of the repair deficient mutants mei-9/sup a/, mei-41/sup D5/, mus101/sup D1/, mus104/sup D1/, and mus302/sup D1/ of Drosophila melanogaster on x-ray induced chromosome loss and translocations in the paternal genome

Thesis/Dissertation ·
OSTI ID:6047779

Each mutant was incorporated singly into ring-x males each provided with V/sup s/Yy/sup +/. From matings of males carrying mus101/sup D1/, mus302/sup D1/, or mei-41/sup D5/, mutants identifying a caffeine sensitive (CAS) postreplication repair pathway, with corresponding mutant females, overall frequencies of spontaneous partial loss and spontaneous complete loss were significantly increased over nonmutant controls. Similar findings were noted when males carrying the excision repair mutant mei-9/sup a/ were mated with mei-9/sup a/ females. Males carrying the mutant mus104/sup D1/, identifying a caffeine insensitive (CIS) postreplication repair pathway, tested with mus104/sup D1/ females, produced results that were not significantly different from non-mutant controls. When males were given 3000 rads x-irradiation, frequencies of induced partial loss were significantly higher with mus101/sup D1/, mus302/sup D1/, mei-41/sup D5/, and mei-9/sup a/ and not significantly different from controls with mus104/sup D1/. It was suggested that the functional CAS postreplication repair pathway primarily promotes repair, while an alternative pathway(s), not defined by mus104/sup D1/, promotes misrepair. Therefore, the significant increases in both spontaneous and induced partial loss with the excision repair deficient mutant mei-9/sup a/ suggest the possibility that (a) the excision repair pathway may not function in misrepair and (b) the undefined misrepair pathway may be the dominant pathway for postreplication repair in Drosophila since mei-9/sup a/ females presumably have functional repair and misrepair capacity.

Research Organization:
Brown Univ., Providence, RI (USA)
OSTI ID:
6047779
Resource Relation:
Other Information: Thesis (Ph. D.)
Country of Publication:
United States
Language:
English