CELL DIVISION AND SURFACE GROWTH IN A "MODEL" SYSTEM

“模型”系统中的细胞分裂和表面生长

• 批准号: 3124870
• 负责人: MICHAEL L HIGGINS
• 金额: $ 12.39万
• 依托单位: TEMPLE UNIV OF THE COMMONWEALTH
• 依托单位国家: 美国
• 财政年份: 1978
• 资助国家: 美国
• 起止时间: 1978-05-01 至 1988-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3124870
• 关键词: Enterococcus; bacterial genetics; biological models; cell cycle; cell growth regulation; cell wall; density gradient ultracentrifugation; developmental genetics; electron microscopy; macromolecule; membrane activity; radiotracer

Two interrelated models have been presented which describe: 1) the regulation of surface growth of Streptococcus faecalis by chromosome replication; and 2) a shape-determining mechanism which directs the assembly of envelope precursors into new cell surface. The first model provides that during a round of chromosome synthesis a signal is produced which results in the formation of a growth zone. This site, once formed, enlarges the cell surface until a second signal, produced during the terminal stages of chromosome replication, inhibits enlargement and promotes septation. The second model is concerned with the construction and function of the growth zone once it has been formed. This model suggests that surface growth proceeds by a regulated flow of cell wall precursors into a growth zone essentially along two channels. One channel would assemble a bilayered cross wall (possibly by the addition of precursors to the leading edge of the cross wall), while a second channel of precursors would convert this cross wall into two layers of peripheral wall. Under the influence of the chromosome termination signal, the flow of precursors along this second channel would be progressively reduced in the latter portion of the cycle. This reduction coupled with the continued flow of precursors into cross wall synthesis could result in cell division. Methods have been devised which can compare the geometry of the envelope with the macromolecular content and autolytic activity of cells. In attempting to test many aspects of the above models, these methods will be applied to steady-state, synchronous, and unbalanced populations where specific inhibition of DNA, RNA, protein, or wall biosynthesis has been induced.

已经提出了两个相互关联的模型，描述了：1） 粪链球菌通过染色体复制在表面生长；和 2) 一个 指导包膜前体组装的形状决定机制 进入新的细胞表面。 第一个模型规定，在一轮染色体合成过程中，信号是 产生，导致生长区的形成。 这个网站，曾经 形成，扩大细胞表面，直到在该过程中产生第二个信号 染色体复制的末期，抑制扩大并促进 分隔。 第二个模型涉及增长的构造和功能 区一旦形成。 该模型表明表面生长继续进行 通过细胞壁前体的调节流进入生长区，基本上沿着 两个通道。 一个通道将组装双层横墙（可能是通过 将前体添加到横壁的前缘），同时 前体的第二个通道会将这个横壁转化为两层 周壁。 在染色体终止信号的影响下， 沿着第二条通道的前体流将逐渐减少 周期的后一部分。 这种减少加上持续的流动 前体进入跨壁合成可能导致细胞分裂。 已经设计出可以将封套的几何形状与 细胞的大分子含量和自溶活性。 在试图 测试上述模型的许多方面，这些方法将应用于 稳态、同步和不平衡群体，其中特异性抑制 DNA、RNA、蛋白质或细胞壁生物合成已被诱导。