The beta 3-tubulin gene of Drosophila melanogaster is essential for viability and fertility.
The beta 3-tubulin gene of Drosophila melanogaster is essential for viability and fertility.
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黑腹果蝇的 β3-微管蛋白基因对于生存力和生育能力至关重要。
DOI：
10.1093/genetics/126.4.991
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发表时间：
1990
期刊：
影响因子：
3.3
通讯作者：
Raff,EC
中科院分区：
文献类型：
--
作者：
Kimble,M;Dettman,RW;Raff,EC
我们以前已经表明，β 3-微管蛋白基因的果蝇编码一个不同的异构体表达在一个复杂的发展模式。β 3基因在胚胎中瞬时表达，在发育中的肌肉组织中以高水平再次在蛹中瞬时表达，在几种不同的外胚层来源的蛹组织中以较低水平瞬时表达。成体表达仅限于性腺中的特定体细胞。在某些表达β 3的细胞类型中，β 3是唯一或主要的β-微管蛋白，而在其他细胞类型中，β 3蛋白是β-微管蛋白库的次要组分。β 3表达的位点和时间表明，β 3-微管蛋白主要用于参与细胞形状和组织结构变化的细胞质微管阵列中，并向我们表明这种亚型可能是功能特化的。为了确定β 3基因的表达是否是正常发育所必需的，并检查这种不同亚型的特定功能，我们在基因内产生了突变。我们确定Df（2 R）Px 2的小缺陷缺失2号染色体的60 C5，6- 60 D9，10区域，去除了所有β 3编码序列，并且缺陷的远端断点在β 3基因转录起始上游约2kb处。我们总共产生了31个甲基磺酸乙酯或二环氧丁烷诱导的隐性致死或可见突变，这些突变在缺陷中映射。这些突变定义了12个新的致死互补组，它们与先前鉴定的两个可见突变一起，在第二染色体的该区间中总共鉴定了14个基因。通过经由P元件介导的生殖系转化引入基因组的基因的野生型拷贝拯救其致死性来鉴定包含β 3-微管蛋白基因（β Tub 60 D）中的突变的致死互补组。对回收的5个β 3突变（等位基因命名为B3 t1-B3 t5）的纯合和转杂合表型的分析表明，β 3-微管蛋白对生存力和生育力至关重要。
We have previously shown that the beta 3-tubulin gene of Drosophila melanogaster encodes a divergent isoform expressed in a complex developmental pattern. The beta 3 gene is transiently expressed in the embryo and again in the pupa at high levels in the developing musculature, and at lower levels in several different pupal tissues of ectodermal origin. Adult expression is confined to specific somatic cells in the gonads. In some of the cell types in which it is expressed, beta 3 is the sole or predominant beta-tubulin, while in others the beta 3 protein is a minor component of the beta-tubulin pool. The sites and timing of beta 3 expression demonstrated that beta 3-tubulin is utilized primarily in cytoplasmic microtubule arrays involved in changes in cell shape and tissue organization, and suggested to us that this isoform may be functionally specialized. To determine whether the expression of the beta 3 gene is essential for normal development, and to examine the specific functions of this divergent isoform, we have generated mutations within the gene. We determined that the small deficiency Df(2R)Px2, which deletes the 60C5,6-60D9,10 region of chromosome 2, removes all of the beta 3 coding sequences, and that the distal breakpoint of the deficiency is approximately 2 kb upstream from the start of transcription of the beta 3 gene. We have generated a total of 31 ethyl methanesulfonate- or diepoxybutane-induced recessive lethal or visible mutations which map within the deficiency. These mutations define 12 new lethal complementation groups, which together with two previously identified visible mutations, altogether identify 14 genes in this interval of the second chromosome. A lethal complementation group comprising mutations in the beta 3-tubulin gene (beta Tub60D) was identified by rescue of their lethality by a wild-type copy of the gene introduced into the genome via P element-mediated germ line transformation. Analysis of the homozygous and transheterozygous phenotypes of the five beta 3 mutations recovered (alleles designated B3t1-B3t5) demonstrates that beta 3-tubulin is essential for viability and fertility.