UNC-33L partially rescues life span and locomotion defects in unc-33 mutants but fails to rescue dauer formation defects.
UNC-33L partially rescues life span and locomotion defects in unc-33 mutants but fails to rescue dauer formation defects.
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DOI：
10.17912/micropub.biology.000515
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发表时间：
2022
影响因子：
--
通讯作者：
Holgado A
中科院分区：
文献类型：
--
作者：
Lopez ME;Vacio AM;Cantu J;Holgado A
在这里，我们测试了UNC-33L修复UNC-33(Mn407)突变体的Dauer形成、寿命和运动缺陷的能力。结果表明，UNC-33L的存在不能挽救UNC-33(Mn407)突变体中的缺陷Dauer表型。然而，UNC-331显著挽救了年轻的UNC-33(Mn407)成年人的过早死亡和不协调的运动。随着线虫年龄的增长，UNC-331介导的救援程度变得不那么明显，这表明年龄和UNC-33L的存在在表型的产生中是相互作用的。
Herein, we tested the ability of UNC-33L to rescue dauer formation, lifespan, and locomotion defects of unc-33(mn407) mutants. Results show that the presence of UNC-33L does not rescue the defective dauer phenotype in unc-33(mn407) mutants. However, UNC-33L significantly rescued premature death and uncoordinated locomotion in young unc-33(mn407) adults. The degree of UNC-33L-mediated rescue was less noticeable as the nematodes aged, denoting that both age and the presence of UNC-33L interact in the production of the phenotypes.