3 ENU-INDUCED ALLELES OF THE MURINE QUAKING LOCUS ARE RECESSIVE EMBRYONIC LETHAL MUTATIONS
3 ENU-INDUCED ALLELES OF THE MURINE QUAKING LOCUS ARE RECESSIVE EMBRYONIC LETHAL MUTATIONS
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DOI：
10.1017/s0016672300024101
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发表时间：
1988-04-01
影响因子：
1.5
通讯作者：
BODE, VC
中科院分区：
文献类型：
--
作者：
JUSTICE, MJ;BODE, VC
小鼠17号染色体上的quaking（qk）基因座已被定义为一个单一的可行的quaking等位基因。ENU诱变后，通过它们不能补充震颤表型，选择了三个新的震颤等位基因。在野生型染色质上诱导qkk 2等位基因，在t染色质上诱导qkkt 1和qkkt 4等位基因。每一个都是隐性胚胎致死突变。它们不能彼此互补，并且不能通过缺失TtOrl互补。纯合子和半合子在妊娠8-9.5天死亡，但不是在一个精确的时间。由于经典的震颤突变补充了这些新等位基因的致死性，但它们未能补充其震颤表型（髓鞘形成缺陷），我们得出结论，震颤+功能是胚胎存活以及髓鞘形成所必需的。
The quaking (qk) locus on mouse chromosome 17 has been defined by a single viable quaking allele. Three new alleles of quaking were selected after ENU mutagenesis by their failure to complement the quaking phenotype. The qkk2 allele was induced on wild-type chromatin and the qkktl and qkkt4 alleles were induced on t-chromatin. Each is a recessive embryonic lethal mutation. They fail to complement each other and are not complemented by the deletion, TtOrl. Homozygotes and hemizygotes die at 8-9.5 days gestation, but not at a single precise time. Because the classical quaking mutation complements the lethality of these new alleles, but they fail to complement its quaking phenotype (myelination defect), we conclude that the quaking+ function is required for embryonic survival as well as for myelination.