Characterization of a new oda3 allele, oda3-6, defective in assembly of the outer dynein arm-docking complex in Chlamydomonas reinhardtii.

Characterization of a new oda3 allele, oda3-6, defective in assembly of the outer dynein arm-docking complex in Chlamydomonas reinhardtii.
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DOI:
10.1371/journal.pone.0173842
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发表时间:
2017
期刊:
影响因子:
3.7
通讯作者:
Wirschell M
Wirschell M
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Brown JM;Mosley M;Montes-Berrueta D;Hou Y;Yang F;Scarbrough C;Witman GB;Wirschell M

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我们使用插入诱变方法来产生新的莱茵衣藻运动突变体。在分离的 56 个突变体中,有一个是 ODA3 基因座上的新等位基因,称为 oda3-6。与之前表征的 oda3 等位基因类似,oda3-6 具有缓慢的急速游泳表型和降低的游泳速度。 oda3-6突变体无法在纤毛轴丝中组装外动力蛋白臂马达和外动力蛋白臂对接复合体(ODA-DC),因为DCC1基因的5'端插入,该基因编码ODA-DC的DC1亚基。用野生型 DCC1 基因转化 oda3-6 可挽救突变游泳表型,并恢复 ODA-DC 和纤毛中外动力蛋白臂的组装。这是第一个在分子水平上表征的 oda3 突变体,可能对于进一步分析 DC1 功能非常有用。
We have used an insertional mutagenesis approach to generate new C. reinhardtii motility mutants. Of 56 mutants isolated, one is a new allele at the ODA3 locus, called oda3-6. Similar to the previously characterized oda3 alleles, oda3-6 has a slow-jerky swimming phenotype and reduced swimming speed. The oda3-6 mutant fails to assemble the outer dynein arm motor and outer dynein arm—docking complex (ODA-DC) in the ciliary axoneme due to an insertion in the 5’ end of the DCC1 gene, which encodes the DC1 subunit of the ODA-DC. Transformation of oda3-6 with the wild-type DCC1 gene rescues the mutant swimming phenotype and restores assembly of the ODA-DC and the outer dynein arm in the cilium. This is the first oda3 mutant to be characterized at the molecular level and is likely to be very useful for further analysis of DC1 function.