Cripps R M, Ball E, Stark M, Lawn A, Sparrow J C
Department of Biology, University of York, England.
Genetics. 1994 May;137(1):151-64. doi: 10.1093/genetics/137.1.151.
To identify further mutations affecting muscle function and development in Drosophila melanogaster we recovered 22 autosomal dominant flightless mutations. From these we have isolated eight viable and lethal alleles of the muscle myosin heavy chain gene, and seven viable alleles of the indirect flight muscle (IFM)-specific Act88F actin gene. The Mhc mutations display a variety of phenotypic effects, ranging from reductions in myosin heavy chain content in the indirect flight muscles only, to reductions in the levels of this protein in other muscles. The Act88F mutations range from those which produce no stable actin and have severely abnormal myofibrillar structure, to those which accumulate apparently normal levels of actin in the flight muscles but which still have abnormal myofibrils and fly very poorly. We also recovered two recessive flightless mutants on the third chromosome. The remaining five dominant flightless mutations are all lethal alleles of a gene named lethal(3)Laker. The Laker alleles have been characterized and the gene located in polytene bands 62A10,B1-62B2,4. Laker is a previously unidentified locus which is haplo-insufficient for flight. In addition, adult wild-type heterozygotes and the lethal larval trans-heterozygotes show abnormalities of muscle structure indicating that the Laker gene product is an important component of muscle.
为了进一步鉴定影响黑腹果蝇肌肉功能和发育的突变,我们获得了22个常染色体显性飞行缺陷突变。从中我们分离出了肌肉肌球蛋白重链基因的8个存活和致死等位基因,以及间接飞行肌(IFM)特异性Act88F肌动蛋白基因的7个存活等位基因。Mhc突变表现出多种表型效应,从仅间接飞行肌中肌球蛋白重链含量的减少到其他肌肉中该蛋白水平的降低。Act88F突变的范围从那些不产生稳定肌动蛋白且肌原纤维结构严重异常的突变,到那些在飞行肌中积累明显正常水平的肌动蛋白但仍有异常肌原纤维且飞行能力很差的突变。我们还在第三条染色体上获得了两个隐性飞行缺陷突变体。其余5个显性飞行缺陷突变都是一个名为lethal(3)Laker基因的致死等位基因。已经对Laker等位基因进行了表征,并将该基因定位在多线带62A10、B1 - 62B2、4处。Laker是一个以前未被鉴定的基因座,其单倍体对飞行是不足的。此外,成年野生型杂合子和致死幼虫反式杂合子显示出肌肉结构异常,表明Laker基因产物是肌肉的重要组成部分。