عنوان

Genetic interactions between DNA gyrase and histone-like protein, HU

Number

TLpq304212066

.Language of Text, Soundtrack etc

انگلیسی

Title Proper

Genetic interactions between DNA gyrase and histone-like protein, HU

General Material Designation

[Thesis]

First Statement of Responsibility

M. R. A. Malik

Subsequent Statement of Responsibility

K. Drlica

Name of Publisher, Distributor, etc.

New York University

Date of Publication, Distribution, etc.

1995

Specific Material Designation and Extent of Item

145

Dissertation or thesis details and type of degree

Ph.D.

Body granting the degree

New York University

Text preceding or following the note

1995

Text of Note

Mutants of Escherichia coli lacking HU, the bacterial histone-like protein, were hypersensitive to novobiocin and grew slowly. The absence of HU created a stress that resulted in decreased spacing of gyrase on chromosomal DNA. Supercoiling comparisons showed that chromosomal supercoiling decreased in the absence of HU. Cultures acquired fast-growing suppressor mutations and lost hypersensitivity to novobiocin. Spontaneous suppressors mapped primarily in the region of gyrB (one such suppressor correlated with an amino acid alteration in GyrB). An HU-deficiency was also suppressed by several other alterations in gyrB: (1) by a pair of known mutations, gyrB203(Ts) gyrB221(Nov at permissive temperature (30C), (2) by a gyrB-expressing plasmid and (3) by a gyrB mutation in conjunction with a gyrA suppressor mutation. These results suggest that HU is involved in maintaining DNA topology through gyrase function. Allele specificity was seen among the gyrB suppressor mutations. Suppressors of an HU deficiency did not suppress a topA deficiency and vice versa. The deficiency of HU in E. coli had a variety of physiological effects. It appeared that gyrase mutations fully suppressed some phenotypes, such as colony size on agar plates and growth rate in LB. However, these mutations only partially suppressed other phenotypes, such as resistance to novobiocin, restoration of normal cell length, and recovery of normal supercoiling. In other cases, such as bacteriophage Mu replication, gyrB suppressors had no effect. Thus there is a multiplicity of interactions: HU sometimes interacts with gyrase but not for all of HU's activities.

Biological sciences

Genetics

Microbiology

novobiocin

K. Drlica

M. R. A. Malik

Electronic name

p

[Thesis]

276903

a

Y