Cooper S F, Zimmering S
Mutat Res. 1981 May;81(3):345-56. doi: 10.1016/0027-5107(81)90121-4.
The repair-deficient mutants mei-9a, mei-41D5, mus101D1, mus104D1 and mus302D1 in Drosophila melanogaster were investigated regarding their effects on spontaneous and X-ray-induced chromosome loss in postmeiotic cells. Each mutant was incorporated singly into XC2, and the ring-X male provided with BSYy+. From matings of males carrying mus101D1, mus302D1 or mei-41D5, mutants identifying a caffeine-sensitive (CAS) postreplication-repair pathway, with corresponding mutant females, and non-mutant males to non-mutant females, overall frequencies of spontaneous partial loss and spontaneous complete loss were significantly increased in each mutant cross except for spontaneous complete loss with mus302 where an increase was noted only in brood 2. Similar findings were noted when males carrying the excision-repair mutant mei-9a were mated with mei-9a females. Males carrying the mutant mus104D1, identifying a caffeine-insensitive (CIS) postreplication-repair pathway, tested with mus104D1 females, produced results that were not significantly different from non-mutant controls. When males were given 3000 rad X-irradiation, frequencies of induced partial loss were significantly higher with mus101D1, mus302D1, mei-41D5 and mei91, and not significantly higher with mus101D1, mus302D1, mei41D5 and mei-9a, and not significantly different from controls with mus104D1. It was suggested that the functional CAS postreplication-repair pathway primarily promotes repair of breaks while an alternative pathway(s) not defined by mus104 promotes misrepair. Therefore, the significant increases in both spontaneous and induced partial loss with the excision-repair-deficient mutant mei-9a suggests the possibility that (a) the excision-repair-pathway may not function in misrepair and (b) the undefined misrepair pathway may be dominant pathway for postreplication repair in Drosophila since mei-9a females presumably have functional postreplication repair and misrepair capacity. The suggestion that the CAS postreplication-repair pathway and the excision-repair pathway function primarily in repair, and an undefined pathway in misrepair is in line with the finding that with mus104D1, no significant increase was found in spontaneous complete loss, but with mus101D1, mus302D1, mei-41D5 and mei-9a significant increases were observed. Results on induced complete loss, with the exception of those with mei-41D5, show a poor correlation with other classes of loss of each of the mutants. Possible explanations for this discrepancy are discussed.
对果蝇中修复缺陷型突变体mei - 9a、mei - 41D5、mus101D1、mus104D1和mus302D1进行了研究，以考察它们对减数分裂后细胞中自发和X射线诱导的染色体丢失的影响。每个突变体单独导入XC2，并为环形X染色体雄性提供BSYy +。携带mus101D1、mus302D1或mei - 41D5（这些突变体确定了一条对咖啡因敏感的（CAS）复制后修复途径）的雄性与相应的突变体雌性以及非突变体雄性与非突变体雌性进行交配，除了mus302D1的自发完全丢失情况（仅在第2窝中观察到增加）外，每个突变体杂交组合中自发部分丢失和自发完全丢失的总体频率均显著增加。当携带切除修复突变体mei - 9a的雄性与mei - 9a雌性交配时，也观察到了类似的结果。携带确定了一条对咖啡因不敏感的（CIS）复制后修复途径的突变体mus104D1的雄性与mus104D1雌性进行测试，其结果与非突变体对照无显著差异。当雄性接受3000拉德X射线照射时，mus101D1、mus302D1、mei - 41D5和mei91诱导的部分丢失频率显著更高，而mus101D1、mus302D1、mei41D5和mei - 9a则没有显著更高，且与mus104D1的对照无显著差异。有人提出，功能性的CAS复制后修复途径主要促进断裂的修复，而mus104未定义的另一条途径则促进错配修复。因此，切除修复缺陷型突变体mei - 9a的自发和诱导部分丢失均显著增加，这表明：（a）切除修复途径可能在错配修复中不起作用；（b）未定义的错配修复途径可能是果蝇复制后修复的主要途径，因为mei - 9a雌性大概具有功能性的复制后修复和错配修复能力。认为CAS复制后修复途径和切除修复途径主要在修复中起作用，而未定义的途径在错配修复中起作用，这与以下发现一致：对于mus104D1，自发完全丢失没有显著增加，但对于mus101D1、mus302D1、mei - 41D5和mei - 9a，则观察到显著增加。除mei - 41D5外，诱导完全丢失的结果与每个突变体的其他类型丢失的相关性较差。文中讨论了这种差异的可能解释。
