An unknown regulator affects cell division and the timing of entry into stationary phase in Escherichia coli

by Bain, Sherrie Valarie

Abstract (Summary)
When an essential nutrient is depleted from the medium, cultures of wildtype

E. coli cells enter a period called stationary phase. The transition into

stationary phase is marked by distinct changes in cell physiology, gene

expression, and morphology. Pr???? and Matsumura (18) found a mutant strain of

E. coli that was able to continue growing exponentially at a time when wild-type

cells had stopped growing and entered stationary phase. They concluded that

FlhD, a transcriptional activator of flagellar genes, was responsible for this

growth phenotype and that it is a regulator of cell division (17, 18). Contrary to

the findings of Pr???? and Matsumura, research in our lab has shown that the

mutant growth phenotype observed in the strain used by Matsumura and Pr???? is

flhD independent. This study sought to identify the second mutation, which we

call cdr (cell division regulator) in the strain used by Matsumura and Pr????. We

used Hfr mapping and P1 transduction to localize the mutation to a specific

region of the chromosome. We also sought to determine if this growth

phenotype was due to loss of function or gain of function and whether the

mutation in the cdr gene was sufficient to cause the observed growth phenotype

in other strain backgrounds. In addition the growth phenotype of these two

strains was compared to that of other wild-type and standard laboratory E. coli

strains. Our results indicate that the cdr mutation is located in the 88.5. region of

the chromosome and is due to loss of Cdr function. We also discovered that the

growth phenotype assigned to the mutant strain more closely reflects that of

other wild-type laboratory strains as did the morphology of cells in stationary

phase. This evidence suggests that the actual mutant strain might be the one

that was designated as the wild-type strain by Matsumura and Pr???? and both

strains may contain mutations that actually cause a decrease in cell number

instead of an increase as previously reported.

Bibliographical Information:

Advisor:Siegele, Deborah A.; Ficht, Thomas A.; Garcia, Rene L.; Sweet, Merrill

School:Texas A&M University

School Location:USA - Texas

Source Type:Master's Thesis

Keywords:unknown regulator


Date of Publication:05/01/2005

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