2 DROSOPHILA LEARNING MUTANTS, DUNCE AND RUTABAGA, PROVIDE EVIDENCE OF A MATERNAL ROLE FOR CAMP ON EMBRYOGENESIS
2 DROSOPHILA LEARNING MUTANTS, DUNCE AND RUTABAGA, PROVIDE EVIDENCE OF A MATERNAL ROLE FOR CAMP ON EMBRYOGENESIS
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DOI：
10.1016/0012-1606(87)90180-1
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发表时间：
1987-06-01
影响因子：
2.7
通讯作者：
KIGER, JA
中科院分区：
文献类型：
--
作者：
BELLEN, HJ;GREGORY, BK;KIGER, JA
黑腹果蝇的dunce基因编码cAMP特异性磷酸二酯酶（II型）。突变的dunce果蝇具有升高的cAMP水平，并表现出许多缺陷，包括学习缺陷和雌性不育。在一个含有dunce无效突变的X染色体上选择了两个雌性不育表型的部分抑制基因。这两种抑制因子都与AC 2活性降低有关。互补分析表明，这两个等位基因的学习突变芜菁。缺失PDE活性的dunce无效突变的纯合子雌性不产存款。抑制剂表现出不同的影响，鸡蛋沉积和生产的后代;双突变的女性存款许多鸡蛋，未能孵化，但有些发展到成年这些成年后代表现出形态缺陷，主要局限于第二和第三胸段或前五个腹段。这些观察结果表明，dunce基因是成年雌性产卵所必需的，并且dunce基因提供了受精卵正常发育所需的基本母性功能。克隆分析，采用显性雌性不育突变ovoD 1，表明前者的PDE活性的要求驻留在体细胞和后者的要求驻留在生殖系细胞。女性生殖细胞纯合子的无效突变产生的卵母细胞不能发育。因此，纯合子的杜斯无效突变合子发育成成年人完全是因为酶或mRNA存在于杂合子母亲的卵母细胞中。芜菁的突变等位基因在生殖细胞中起作用，部分抑制由笨蛋突变引起的发育缺陷。因此，芜菁基因和dunce基因在体细胞和生殖细胞中都发挥作用。
The dunce gene of Drosophila melanogaster encodes a cAMP-specific phosphodiesterase (form II). Mutant dunce flies have elevated levels of cAMP and exhibit a number of defects including learning deficiencies and female sterility. Two partial suppressors of the female sterility phenotype have been selected in an X chromosome containing a dunce null mutation. Both suppressors are associated with reduced AC2 activity. Complementation analyses suggest that both are alleles of the learning mutant rutabaga. Females homozygous for dunce null mutations that abolish PDE activity do not deposit eggs. The suppressors exhibit differential effects on egg deposition and production of progeny; double-mutant females deposit many eggs that fail to hatch, but some develop to adult these adult progeny exhibit morphological defects that are confined mostly to the second and third thoracic segments or to the first five abdominal segments. These observations demonstrate that the dunce gene is required in adult females for egg laying and that the dunce gene provides as essential maternal function required for normal development of the zygote. Clonal analysis, employing the dominant female-sterile mutation ovoD1, demonstrates that the former requirement for PDE activity resides in somatic cells and that the latter requirement resides in germ line cells. Female germ line cells homozygous for a dunce null mutation produce oocytes that fail to develop. Thus, homozygous dunce null-mutant zygotes develop to adults solely because of the enzyme or mRNA present in the oocytes of heterozygous mothers. Mutant alleles of rutabaya act in the germ line cells to partially suppress the developmental defects caused by dunce mutations. Thus the rutabaya gene, as well as the dunce gene, functions in both somatic and germ line cells.