Caberoy Nora B, Welch Roy D, Jakobsen Jimmy S, Slater Steven C, Garza Anthony G
School of Molecular Biosciences, Washington State University, Pullman, Washington 99164-4234, USA.
J Bacteriol. 2003 Oct;185(20):6083-94. doi: 10.1128/JB.185.20.6083-6094.2003.
The multicellular developmental cycle of Myxococcus xanthus requires large-scale changes in gene transcription, and recent findings indicate that NtrC-like activators play a prominent role in regulating these changes. In this study, we made insertions in 28 uncharacterized ntrC-like activator (nla) genes and found that eight of these insertions cause developmental defects. Hence, these results are consistent with the idea that M. xanthus uses a series of different NtrC-like activators during fruiting body development. Four of the eight developmental mutants we identified have motility defects. The nla1, nla19, and nla23 mutants show S-motility defects, while the nla24 mutant shows defects in both S-motility and A-motility. During development, aggregation of the nla1, nla19, and nla23 mutants is delayed slightly and the nla24 mutant shows no signs of aggregation or sporulation. The nla4, nla6, nla18, and nla28 mutants have no appreciable loss in motility, but they fail to aggregate and to sporulate normally. The nla18 mutant belongs to a special class of developmental mutants whose defects can be rescued when they are codeveloped with wild-type cells, suggesting that nla18 fails to produce a cell-cell signal required for development. The three remaining activator mutants, nla4, nla6, and nla28, appear to have complex developmental phenotypes that include deficiencies in cell-cell developmental signals.
黄色粘球菌的多细胞发育周期需要基因转录发生大规模变化,最近的研究结果表明,NtrC样激活因子在调节这些变化中发挥着重要作用。在本研究中,我们在28个未表征的NtrC样激活因子(nla)基因中进行了插入,发现其中8个插入导致发育缺陷。因此,这些结果与黄色粘球菌在子实体发育过程中使用一系列不同的NtrC样激活因子这一观点一致。我们鉴定出的8个发育突变体中有4个具有运动缺陷。nla1、nla19和nla23突变体表现出S型运动缺陷,而nla24突变体在S型运动和A 型运动方面均表现出缺陷。在发育过程中,nla1、nla19和nla23突变体的聚集略有延迟,nla24突变体没有聚集或形成孢子的迹象。nla4、nla6、nla18和nla28突变体的运动能力没有明显丧失,但它们无法正常聚集和形成孢子。nla18突变体属于一类特殊的发育突变体,当它们与野生型细胞共同发育时,其缺陷可以得到挽救,这表明nla18无法产生发育所需的细胞间信号。其余三个激活因子突变体nla4、nla6和nla28似乎具有复杂的发育表型,包括细胞间发育信号缺陷。