MUTANTS OF CAENORHABDITIS-ELEGANS THAT FORM DAUER-LIKE LARVAE
MUTANTS OF CAENORHABDITIS-ELEGANS THAT FORM DAUER-LIKE LARVAE
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DOI：
10.1016/0012-1606(88)90138-8
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发表时间：
1988-04-01
影响因子：
2.7
通讯作者：
RIDDLE, DL
中科院分区：
文献类型：
--
作者：
ALBERT, PS;RIDDLE, DL
形成 dauer 样幼虫的两种突变体的发育、超微结构和遗传学已经得到表征。无论环境刺激如何，Dauer幼虫的形态发生都会启动，并且是不完整或异常的。正常 dauer 幼虫对洗涤剂特性的抗性尚未完全实现，并且突变体无法退出类似 dauer 的发育停滞状态。突变体的寿命不会延长超过非dauer生命周期特征的三周，而正常的dauer幼虫可以存活几个月。 daf-15(m81)IV 是两者中不太像 dauer 的一个，在第二次（dauer 特异性）蜕皮时几乎停止生长，但摄食并未完全受到抑制。头部形状、角质层和肠道超微结构是非dauer阶段，而感觉结构（amphid和deirid）和排泄腺形态介于dauer阶段和nondauer阶段之间。 daf-9(e1406)X 突变体的头部形状、角质层和迪虹膜超微结构呈 dauer 状，在两栖动物和内唇神经元形态上处于中间状态，在肠道中呈非 dauer 或异常。此外，daf-9突变体在咽部拱廊细胞突起和咽部g1腺中表现出异常。同时携带 daf-9 和 daf-15 的双突变体比任一单突变体对洗涤剂具有更强的抵抗力。与单一突变体一样，它们无法完成形态发生，也无法退出类似 dauer 的阶段。 daf-9 和 daf-15 突变均与先前描述的 dauer 缺陷突变上位，表明这两个基因在通往 dauer 幼虫的途径中发挥作用较晚。基因测试和突变超微结构表明这两个基因可能影响形态发生的平行途径。
The development, ultrastructure, and genetics of two mutants that form dauer-like larvae have been characterized. Dauer larva morphogenesis is initiated regardless of environment stimuli, and its is incomplete or abnormal. The resistance to detergent chracterisitc of normal dauer larvae is not fully achieved, and the mutants are unable to exit fromthe dauer-like state of developmental arrest. Mutant life span is not extended beyond the three weeks characteristic of the nondauer life cycle, whereas normal dauer larvae can live for several months. Growth of daf-15(m81)IV, the less dauer-like of the two, is nearly arrested at the second (dauer-specific) molt, but feeding is not completely suppressed. Head shape, cuticle, and intestinal ultrastructure are nondauer, whereas sensory structures (amphid and deirid) and excretory gland morphology are intermdiate between that of dauer and nondauer stages. The daf-9(e1406)X mutant is dauer-like in head shape, cuticle, and deirid ultrastructure, intermediate in amphid and inner labial neuron morphology, and nondauer or abnormal in the intestine. Also, the daf-9 mutant exhibits abnormailites in the pharyngeal arcade cell processes and pharyngeal g1 gland. Double mutants carrying both daf-9 and daf-15 are more resistant to detergent than either single mutant. Like the single mutants, they cannot complete morphogenesis, and they are unable to exit from the dauer-like stage. Both daf-9 and daf-15 mutations are epistatic to previously described dauer-defective mutations, indicating that these two genes act late in the pathway leading to the dauer larva. The genetic test and the mutant ultrastructure suggest that the two genes may affect parallel pathways of morphogenesis.