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Mas Transit: A GTPase and kinase membrane protein complex regulate gliding in Myxococcus xanthus.

机译:Mas Transit:一种GTPase和激酶膜蛋白复合物,可调节黄色粘球菌的滑动。

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摘要

Myxococcus xanthus is a Gram-negative social prokaryote that utilizes gliding motility. Adventurous (A) and social (S) gliding motility are dependent on the expression of over 200 genes that encode motor proteins, sensory systems and extracellular matrix regulators. A and S-motility are required for a complex developmental program that allows M. xanthus to survive conditions of hardship such as heat, desiccation and nutrient starvation. Coordination of these two motility systems is contingent on the function of a Ras-like GTPase, MglA. MglA activity requires GTP-nucleotide binding and hydrolysis, which depends upon conserved residues in consensus motifs PM1, G2 and PM3. GTP hydrolysis is required in order to control downstream signaling proteins in both A and S motors. Although the PM3 consensus has some conservation to Ras, MglA has a threonine present at position 78, and engineering PM3 to match the Ras T78D consensus results in stable, but nonfunctional MglA.;An mglA allele, mglA8, is nonmotile (A-S-). The S-motility phenotype can be partially suppressed by a second-site mutation in the masK gene. MasK is a known serine-threonine-tyrosine protein kinase required for S-motility. Upstream of masK are two genes, masA and masB, which are cotranscribed in one polycistronic mRNA with masK. MasA appears to be an integral inner membrane protein while MasB is a putative lipoprotein. Deletion of the masABK operon specifically affects S-motility, swarming, gliding velocity and development. The deletion in masABK abolished pilA expression without causing detectable mutation at the pilA locus. Addition of a wild-type (WT) copy of pilA restored social motility to nearly 40% of WT, while swarming was restored to 78% of WT. Development was restored only in a ΔmasABK strain complemented with pilA and masABK. Epigenetic silencing or second-site mutations may be responsible for an inability of masABK to complement the masABK deletion.
机译:黄色粘球菌是利用滑行运动的革兰氏阴性社交原核生物。冒险(A)和社交(S)滑行运动取决于200多个编码运动蛋白,感觉系统和细胞外基质调节剂的基因的表达。 A和S活力是一项复杂的发展计划所必需的,该计划可使黄花棘枝to得以忍受艰苦的条件,例如高温,干燥和营养缺乏。这两个运动系统的协调取决于Ras样GTP酶MglA的功能。 MglA活性需要GTP核苷酸结合和水解,这取决于共有基序PM1,G2和PM3中的保守残基。需要GTP水解以控制A和S马达中的下游信号蛋白。尽管PM3共有蛋白对Ras具有一定的保守性,但MglA在78位上存在苏氨酸,工程改造PM3以使其与Ras T78D共有蛋白相匹配会产生稳定但无功能的MglA。; mglA等位基因mglA8是不运动的(A-S-)。可由masK基因中的第二个位点突变部分抑制S运动型。 MasK是S运动所需的一种已知的丝氨酸-苏氨酸-酪氨酸蛋白激酶。 masK的上游有两个基因masA和masB,它们与masK在一个多顺反子mRNA中共转录。 MasA似乎是不可或缺的内膜蛋白,而MasB是推定的脂蛋白。删除masABK操纵子会特别影响S活力,群聚,滑行速度和发育。 masABK的缺失消除了pilA表达,而没有引起pilA基因座的可检测突变。加入野生型pilA副本可将社会活力恢复到WT的近40%,而蜂群则恢复到WT的78%。仅在补充了pilA和masABK的ΔmasABK菌株中恢复了发育。表观遗传沉默或第二位点突变可能是masABK无法补充masABK缺失的原因。

著录项

  • 作者

    Fremgen, Sarah Anne.;

  • 作者单位

    University of Idaho.;

  • 授予单位 University of Idaho.;
  • 学科 Biology Molecular.;Biology Microbiology.
  • 学位 Ph.D.
  • 年度 2012
  • 页码 157 p.
  • 总页数 157
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

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