Developmental genetics of the 2C-D region of the Drosophila X chromosome.
Developmental genetics of the 2C-D region of the Drosophila X chromosome.
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果蝇 X 染色体 2C-D 区域的发育遗传学。
DOI：
10.1093/genetics/111.1.23
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发表时间：
1985
期刊：
影响因子：
3.3
通讯作者：
Mahowald,AP
中科院分区：
文献类型：
--
作者：
Perrimon,N;Engstrom,L;Mahowald,AP
我们对X染色体2C-D区域内的基因进行了遗传和发育分析。描述了代表9个相邻互补群的33个突变的表型，其中包括8个隐性致死突变和1个可见的同源异型突变(多同源异型)。对8个合子致死基因的种系克隆分析揭示了三种类型的基因需求：(1)正常胚胎发生需要两个幼虫致死基因座(软木塞和C204)和一个幼虫致死基因座(超阿司匹林)的正常活性；(2)正常卵子发生需要三个幼虫致死基因座(DF967、VE651和Pgd)的正常活性；以及(3)只有一个致死幼虫基因座(EA82)的活性似乎与母体无关。GF316致死互补组的结果不明确。对幼虫有丝分裂形态的分析表明，C204破坏了一种基本的有丝分裂功能。这一结果与在来自C204胚系克隆的胚胎中观察到的前胚层停滞有关。来自开瓶器(CSW)种系克隆的胚胎表现出“扭曲”的表型。隐性致死性超阿司匹林(USP)从受精卵和母体两个方面破坏了幼虫后端的组织：来自杂合子/+母亲的第二个instarusp/Ylarvae拥有一套额外的气孔，而来自拥有生殖系克隆(USP/USP)的雌性胚胎(USP/USP)在第九或后八个腹部节段显示出局限性的腹侧缺陷。对缺陷-半合子胚胎的表型分析表明，存在一个尚未确定的胚胎合子致死基因，该基因可导致中枢神经系统和腹侧皮下组织变性。还描述了有关相邻2E区域内的基因座遗传组织的其他信息。这一分析对我们理解母系发育中合子致死基因座的意义进行了讨论。
We have conducted a genetic and developmental analysis of genes within the 2C-D area of theXchromosome. Phenotypes of 33 mutations representing nine adjacent complementation groups including eight recessive lethals and one visible homeotic mutation (polyhomeotic) are described. Germline clonal analysis of the eight zygotic lethals has revealed three types of gene requirements: (1) normal activity at two pupal lethal loci (corkscrew andC204) and one larval lethal locus (ultraspiracle) is required for normal embryogenesis; (2) normal activity at three larval lethal loci (DF967, VE651andPgd) is required for normal oogenesis; and (3) activity at only one locus (EA82), a larval lethal, appears to have no maternal requirement. Ambiguous results were obtained for theGF316lethal complementation group. Analysis of mitotic figures of the pupal lethals indicates thatC204disrupts an essential mitotic function. This result correlates with the preblastoderm arrest observed among embryos derived from germline clones ofC204. Embryos derived from germline clones of corkscrew (csw) exhibit a "twisted" phenotype. The recessive lethal ultraspiracle (usp) disrupts the organization of the posterior tip of the larva both zygotically and maternally: second instarusp/Ylarvae derived from heterozygoususp/+ mothers possess an extra set of spiracles, whereasusp/Yembryos derived from females possessing a germline clone (usp/usp) exhibit a localized ventral defect in the ninth or posterior eighth abdominal segment. Analysis of the phenotypes of deficiency-hemizygous embryos indicates the presence of an embryonic zygotic lethal locus, as yet unidentified, which produces central nervous system and ventral hypoderm degeneration. Additional information on the genetic organization of loci within the adjacent 2E area are also described. The implications of this analysis to our understanding of the maternal of zygotic lethal loci in development are discussed.