Mutants resistant to anti-microtubule herbicides map to a locus on the uni linkage group in Chlamydomonas reinhardtii.
Mutants resistant to anti-microtubule herbicides map to a locus on the uni linkage group in Chlamydomonas reinhardtii.
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对抗微管除草剂具有抗性的突变体定位于莱茵衣藻单连锁群上的一个基因座。
DOI：
10.1093/genetics/118.1.141
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发表时间：
1988
期刊：
影响因子：
3.3
通讯作者：
Lefebvre,PA
中科院分区：
文献类型：
--
作者：
James,SW;Ranum,LP;Silflow,CD;Lefebvre,PA
我们已经使用遗传分析来研究两种抗微管除草剂，甲基氨丙啶（APM）和安磺灵（ORY）的作用模式。通过在含有APM或ORY的平板上生长，选择了超过200种抗性突变体。在这项研究中检查的21个独立分离的突变体对APM具有3至8倍的抗性，并且对ORY和butamiphos具有强烈的交叉抗性，butamiphos是APM的接近类似物。通过连锁和互补分析确定了两个孟德尔基因apm 1和apm 2。apm 1有20个等位基因，apm 2有一个温度敏感致死（33度）等位基因。通过双因子杂交定位apm 1 6.5 cM的着丝粒近端uni 1和4 cM内的pf 7上的uni连锁群，一个遗传环状连锁群，包括基因，影响鞭毛组装或功能; apm 2地图附近的着丝粒连锁群VIII。在apm 2和apm 1的等位基因之间的杂交中观察到等位基因特异性合成致死性。此外，apm 2的自交是合子致死的，而9个apm 1等位基因的自交导致正常的发芽和四分体活力。突变体是隐性的野生型等位基因，但双杂合二倍体（apm 1 +/+ apm 2）与apm 2和任何15 apm 1等位基因显示部分基因间非互补，表示为中间电阻。apm 1突变等位基因纯合的二倍体对APM和ORY的抗性是4-6倍; apm 2纯合的二倍体对除草剂的抗性是ts-和2倍。双杂合二倍体补充了apM 2的ts-表型，但它们通常对APM和ORY具有1.5-2倍的抗性。从上述结果中，我们认为apm 1和apm 2的基因产物可能直接相互作用或在相同的结构或过程中起作用。
We have used genetic analysis to study the mode of action of two anti-microtubule herbicides, amiprophos-methyl (APM) and oryzalin (ORY). Over 200 resistant mutants were selected by growth on APM- or ORY-containing plates. The 21 independently isolated mutants examined in this study are 3- to 8-fold resistant to APM and are strongly cross-resistant to ORY and butamiphos, a close analog of APM. Two Mendelian genes, apm1 and apm2, are defined by linkage and complementation analysis. There are 20 alleles of apm1 and one temperature-sensitive lethal (33 degrees) allele of apm2. Mapping by two-factor crosses places apm1 6.5 cM centromere proximal to uni1 and within 4 cM of pf7 on the uni linkage group, a genetically circular linkage group comprising genes which affect flagellar assembly or function; apm2 maps near the centromere of linkage group VIII. Allele-specific synthetic lethality is observed in crosses between apm2 and alleles of apm1. Also, self crosses of apm2 are zygotic lethal, whereas crosses of nine apm1 alleles inter se result in normal germination and tetrad viability. The mutants are recessive to their wild-type alleles but doubly heterozygous diploids (apm1 +/+ apm2) made with apm2 and any of 15 apm1 alleles display partial intergenic noncomplementation, expressed as intermediate resistance. Diploids homozygous for mutant alleles of apm1 are 4-6-fold resistant to APM and ORY; diploids homozygous for apm2 are ts- and 2-fold resistant to the herbicides. Doubly heterozygous diploids complement the ts- phenotype of apM2, but they are typically 1.5-2-fold resistant to APM and ORY. From the results described we suggest that the gene products of apm1 and apm2 may interact directly or function in the same structure or process.