Functions of the Caenorhabditis elegans regulatory myosin light chain genes mlc-1 and mlc-2.
Functions of the Caenorhabditis elegans regulatory myosin light chain genes mlc-1 and mlc-2.
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发表时间：
1998-11
期刊：
影响因子：
3.3
通讯作者：
A. Rushforth;C. White;P. Anderson
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作者：
A. Rushforth;C. White;P. Anderson
秀丽隐杆线虫含有两个肌肉调节肌球蛋白轻链基因，mlc-1和mlc-2。为了确定它们在体内的作用，我们鉴定了单独消除每个基因和组合消除两个基因的缺失。在体壁和咽肌中，mlc-1的功能与mlc-2的功能相比是多余的。mlc-1（0）突变体是野生型，但mlc-1（0）mlc-2（0）双突变体作为不完全伸长的L1幼虫停滞，具有咽和体壁肌肉缺陷。mlc-1（+）或mlc-2（+）的转基因拷贝挽救了mlc-1（0）mlc-2（0）双突变体的所有缺陷。在体壁肌肉中，MLC-2相对于MLC-1是多余的，但MLC-2在咽中发挥几乎必要的作用。大约90%的mlc-2（0）两性体由于咽肌缺陷而停滞为L1幼虫。mlc-2（0）突变体的致死率是性别特异性的，mlc-2（0）雄性基本上是野生型。四项观察结果表明，mlc-2（0）突变体的雌雄同体特异性致死性是由咽部X连锁的mlc-1（+）基因表达不足引起的。首先，mlc-1（0）mlc-2（0）双突变体在雌雄同体和雄性中都是完全外显的L1致死。其次，mlc mRNA的原位定位表明mlc-1和mlc-2都在咽部表达。第三，mlc-1（+）或mlc-2（+）的转基因拷贝挽救了mlc-1（0）mlc-2（0）雌雄同体的咽部缺陷。第四，剂量补偿基因sdc-3的突变抑制了mlc-2（0）突变体的雌雄同体特异性致死性。
Caenorhabditis elegans contains two muscle regulatory myosin light chain genes, mlc-1 and mlc-2. To determine their in vivo roles, we identified deletions that eliminate each gene individually and both genes in combination. Functions of mlc-1 are redundant to those of mlc-2 in both body-wall and pharyngeal muscle. mlc-1(0) mutants are wild type, but mlc-1(0) mlc-2(0) double mutants arrest as incompletely elongated L1 larvae, having both pharyngeal and body-wall muscle defects. Transgenic copies of either mlc-1(+) or mlc-2(+) rescue all defects of mlc-1(0) mlc-2(0) double mutants. mlc-2 is redundant to mlc-1 in body-wall muscle, but mlc-2 performs a nearly essential role in the pharynx. Approximately 90% of mlc-2(0) hermaphrodites arrest as L1 larvae due to pharyngeal muscle defects. Lethality of mlc-2(0) mutants is sex specific, with mlc-2(0) males being essentially wild type. Four observations suggest that hermaphrodite-specific lethality of mlc-2(0) mutants results from insufficient expression of the X-linked mlc-1(+) gene in the pharynx. First, mlc-1(0) mlc-2(0) double mutants are fully penetrant L1 lethals in both hermaphrodites and males. Second, in situ localization of mlc mRNAs demonstrates that both mlc-1 and mlc-2 are expressed in the pharynx. Third, transgenic copies of either mlc-1(+) or mlc-2(+) rescue the pharyngeal defects of mlc-1(0) mlc-2(0) hermaphrodites. Fourth, a mutation of the dosage compensation gene sdc-3 suppresses hermaphrodite-specific lethality of mlc-2(0) mutants.