Function of Mg1 Proteins in Gliding in Myxococcus

这个项目的长期目标是了解黏菌表面移位或滑动的机制。包括黏液菌、噬细胞菌、蓝藻菌和Beggiotoa在内的多种环境重要生物的生存取决于它们的滑翔能力。在这个项目中，黄粘球菌将被用作理解滑翔的模型，因为它具有良好的遗传特征。mglA基因对滑翔至关重要；这个项目的重点将是MglA蛋白如何与其他运动成分相互作用。由于mglA是控制滑翔的两个已知遗传鉴定系统A和S的唯一共同基因，因此mglA蛋白可能影响A和S滑翔基因的表达。因此，第一个目标将是分离和表征A-和s -运动基因中的报告基因（lacZ）插入，并确定它们的转录是否在mgl-菌株中发生改变。另一个目标将是利用诱变技术，通过识别显示异常滑动的MglA突变体来探测MglA的功能域。抑制实验也被设计用于识别编码与MglA相互作用的蛋白质的基因。一种抑制mglA缺陷的突变体已经被发现，相应的基因将被克隆，以确定它是否编码一种与mglA相互作用的滑动蛋白。细菌需要能够从一个地方移动到另一个地方才能生存。细菌在固体基质上的滑行现象是最有趣的，也是最不为人所知的运动机制之一。这一领域的复杂之处在于，一组滑翔细菌所使用的滑翔机制可能与其他群体所使用的不同。在黏菌中，滑翔不仅对细菌寻找食物至关重要，而且还能使细菌经历从营养滑翔细菌到产孢“子实体”的发育转变。有两个几乎独立的运动系统，称为“A”（“冒险”）和“S”（“社交”）。s -运动性需要细胞间接近才能发生运动，已知至少涉及12种不同的基因。a -运动性不需要细胞间接触，至少由22个基因控制。野生型黏液球菌具有A+和S+两种运动性。A或S基因中的一个发生突变，只会使A或S型的运动能力丧失。这两种机制似乎都涉及相同的基本运动机制的调节。此外，还有其他基因，称为“frz”基因，它影响细胞在滑行时逆转方向的速度。然而，有一个单一的遗传位点mglA，其突变消除了a型和S型的运动性，导致完全没有运动性的细菌。对这一关键基因的研究可能会为粘球菌的滑翔机制提供新的线索。

The long range goal of this project is to understand the mechanism of surface translocation, or gliding, in myxobacteria. The survival of a diverse group of environmentally important organisms, including myxobacteria, cytophaga, cyanobacteria, and Beggiotoa, depends upon their ability to glide. In this project, Myxococcus xanthus will be used as a model to understand gliding because it is genetically well-characterized. One gene, mglA, is essential for gliding; the focus of this project will be on how MglA protein interacts with other motility components. Since mglA is the only gene common to the two known genetically-identified systems, A and S, that control gliding, MglA protein may affect expression of A- and S-gliding genes. The first aim will therefore be to isolate and characterize reporter gene (lacZ) insertions in A- and S-motility genes and determine if their transcription is altered in an mgl- strain. Another goal will be to use mutagenesis to probe the functional domains of MglA by identifying mglA mutants that show aberrant gliding. Suppressor experiments have also been designed to identify genes encoding proteins that interact with MglA. One mutant has already been identified that suppresses the mglA defect, and the corresponding gene will be cloned to determine if it encodes a gliding protein that interacts with MglA. %%% Bacteria need to be able to move from one place to another in order to survive. One of the most intriguing, and least understood, mechanisms of bacterial motility is the phenomenon of gliding on solid substrata. The field is complicated by the likelihood that the gliding mechanisms employed by one group of gliding bacteria may not be the same as those employed by other groups. In myxobacteria, gliding is crucial not only to enable the bacteria to find food, but also to enable the bacteria to undergo a developmental transition from the vegetative gliding bacterium form to a sporogenic "fruiting body." There are two almost independent motility systems, termed "A" ("adventurous") and "S" ("social"). S-motility requires cell-to-cell proximity for movement to occur, and is known to involve at least 12 distinct genes. A-motility does not require cell-cell contact, and is controlled by at least 22 genes. Wild-type myxococci exhibit both A+ and S+ motility. A mutation in one of the A or S genes abolishes only the A or S type of motility. Both of these mechanisms seem to involve regulation of the same basic motility machinery. In addition, there are other genes, termed "frz" genes, which affect the rate at which cells reverse direction while gliding. However, there is a single genetic locus, mglA, for which a mutation abolishes both A and S type motility, resulting in totally nonmotile bacteria. The proposed studies of this pivotal gene are likely to shed new light on the mechanism of gliding in myxococci.