Waterston R H
Genetics. 1981 Feb;97(2):307-25. doi: 10.1093/genetics/97.2.307.
More than 30 independent suppressor mutations have been obtained in the nematode C. elegans through reversion analysis of two unc-13 mutants. Many of the new isolates map to the region of the previously identified informational suppressor, sup-5 III (WATERSTON and BRENNER 1978). Several of the other suppressor mutations map to the left half of the X-linkage group and define a second suppressor gene, sup-7 X. In tests against 40 mutations in six genes, the sup-7(st5) allele was found to suppress to a greater extent the same alleles acted on by sup-5(e1464). Like sup-5(e1464), sup-7(st5) acts on null alleles of the myosin heavy-chain gene unc-54 I (MACLEOD et al. 1977; MACLEOD, WATERSTON and BRENNER 1977) and the putative paramyosin gene unc-15 I (WATERSTON et al. 1977). Chemical analysis of unc-15(e1214); sup-7(st5) animals show that paramyosin is restored to more than 30% of the wild-type level.--As was observed for sup-5(e1464), suppression by sup-7(st5) is dose dependent and is greater in animals grown at 15 degrees than at 25 degrees. However, associated with this increased suppression is a decreased viability of sup-7(st5) homozygotes. Reversion of the lethality has resulted in the isolation of deficiency mutations that complement st5 lethality, but lack suppressor function. These properties of sup-7(st5) suggest that it, like sup-5(e1464), is an information suppressor of null alleles, and its reversion via deficiencies further narrows the possible explanations of its action.
通过对两个unc-13突变体进行回复分析,已在线虫秀丽隐杆线虫中获得了30多个独立的抑制突变。许多新分离株定位于先前鉴定的信息抑制基因sup-5Ⅲ所在区域(WATERSTON和BRENNER,1978年)。其他几个抑制突变定位于X连锁群的左半部分,并定义了第二个抑制基因sup-7 X。在针对六个基因中的40个突变进行的测试中,发现sup-7(st5)等位基因在更大程度上抑制了sup-5(e1464)作用的相同等位基因。与sup-5(e1464)一样,sup-7(st5)作用于肌球蛋白重链基因unc-54 I(MACLEOD等人,1977年;MACLEOD、WATERSTON和BRENNER,1977年)和推定的副肌球蛋白基因unc-15 I(WATERSTON等人,1977年)的无效等位基因。对unc-15(e1214);sup-7(st5)动物的化学分析表明,副肌球蛋白恢复到野生型水平的30%以上。——正如对sup-5(e1464)所观察到的那样,sup-7(st5)的抑制作用是剂量依赖性的,并且在15摄氏度下生长的动物中比在25摄氏度下更大。然而,伴随着这种抑制作用的增强,sup-7(st5)纯合子的活力降低。致死性的回复导致了缺失突变的分离,这些突变可互补st5致死性,但缺乏抑制功能。sup-7(st5)的这些特性表明,它与sup-5(e1464)一样,是无效等位基因的信息抑制基因,并且通过缺失进行的回复进一步缩小了对其作用的可能解释范围。