Characterization and application of a putative transcription factor (SUT2) in Pichia pastoris

Abstract An ssu2 mutation in Sacccharomyces cermisiae, previously shown to cause sulfite sensitivity, was found to be allelic to GRR1, a gene previously implicated in glucose repression. The suppressor rgt1, which suppresses the growth defects of grr1 strains on glucose, did not fully suppress the sensitivity on glucose or nonglucose carbon sources, indicating that it is not strictly linked to a defect in glucose metabolism. Because the Cln1 protein was previously shown to be elevated in grr1 mutants, the effect of CLN1 overexpression on sulfite sensitivity was investigated. Overexpression in GRR1 cells resulted in sulfite sensitivity, suggesting a connection between CLN1 and sulfite metabolism. Multicopy FZF1, a putative transcription factor, was found to suppress the sulfite sensitive phenotype of grr1 strains, but not the glucose derepression or aberrant cell morphology. Multicopy FZF1 was also found to suppress the sensitivity of a number of other unrelated sulfite-sensitive mutants, but not that of ssu1 or met20, implying that FZF1 may act through Ssulp and Met20p. Disruption of FZF1 resulted in sulfite sensitivity when the construct was introduced in single copy at the FZF1 locus in a GRR1 strain, providing evidence that FZF1 is involved in sulfite metabolism.

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The X-ray crystal structure of PA1607 from Pseudomonas aureginosa at 1.9 A resolution--a putative transcription factor

Protein Science ◽

10.1110/ps.062668207 ◽

2007 ◽

Vol 16 (3) ◽

pp. 543-549 ◽

Cited By ~ 3

Author(s):

E. A.L. Sieminska ◽

X. Xu ◽

A. Savchenko ◽

D. A.R. Sanders

Keyword(s):

Crystal Structure ◽

Transcription Factor ◽

X Ray ◽

Putative Transcription Factor

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Recognition DNA Sequence of a Novel Putative Transcription Factor, BCL6

Biochemical and Biophysical Research Communications ◽

10.1006/bbrc.1994.2468 ◽

1994 ◽

Vol 204 (1) ◽

pp. 366-374 ◽

Cited By ~ 47

Author(s):

N. Kawamata ◽

T. Miki ◽

K. Ohashi ◽

K. Suzuki ◽

T. Fukuda ◽

...

Keyword(s):

Transcription Factor ◽

Dna Sequence ◽

Putative Transcription Factor

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mirror controls planar polarity and equator formation through repression of fringe expression and through control of cell affinities

Development ◽

10.1242/dev.126.24.5857 ◽

1999 ◽

Vol 126 (24) ◽

pp. 5857-5866 ◽

Cited By ~ 5

Author(s):

C.H. Yang ◽

M.A. Simon ◽

H. McNeill

Keyword(s):

Transcription Factor ◽

Expression Pattern ◽

Mirror Image ◽

Sharp Boundary ◽

Planar Polarity ◽

Specific Expression ◽

Mirror Function ◽

Putative Transcription Factor ◽

Specific Expression Pattern ◽

Dorsal Cells

The Drosophila eye is divided into dorsal and ventral mirror image fields that are separated by a sharp boundary known as the equator. We have previously demonstrated that Mirror, a homeodomain-containing putative transcription factor with a dorsal-specific expression pattern in the eye, induces the formation of the equator at the boundary between mirror-expressing and non-expressing cells. Here, we provide evidence that suggests mirror regulates equator formation by two mechanisms. First, mirror defines the location of the equator by creating a boundary of fringe expression at the mid-point of the eye. We show that mirror creates this boundary by repressing fringe expression in the dorsal half of the eye. Significantly, a boundary of mirror expression cannot induce the formation of an equator unless a boundary of fringe expression is formed simultaneously. Second, mirror acts to sharpen the equator by reducing the mixing of dorsal and ventral cells at the equator. In support of this model, we show that clones of cells lacking mirror function tend not to mix with surrounding mirror-expressing cells. The tendency of mirror-expressing and non-expressing cells to avoid mixing with each other is not determined by their differences in fringe expression. Thus mirror acts to regulate equator formation by both physically separating the dorsal cells from ventral cells, and restricting the formation of a fng expression boundary to the border where the dorsal and ventral cells meet.

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KMP049 Overexpression of a novel putative transcription factor (Roh) of Enterobacter cloacae in Escherichia coli increases the MIC to ciprofloxacin >/ = 4fold

International Journal of Medical Microbiology Supplements ◽

10.1016/s1433-1128(03)80931-2 ◽

2003 ◽

Vol 293 ◽

pp. 398-399

Keyword(s):

Escherichia Coli ◽

Transcription Factor ◽

Enterobacter Cloacae ◽

Putative Transcription Factor

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Involvement of the putative hematopoietic transcription factor SCL in T- cell acute lymphoblastic leukemia

Blood ◽

10.1182/blood.v79.5.1327.1327 ◽

1992 ◽

Vol 79 (5) ◽

pp. 1327-1333 ◽

Cited By ~ 73

Author(s):

PD Aplan ◽

DP Lombardi ◽

GH Reaman ◽

HN Sather ◽

GD Hammond ◽

...

Keyword(s):

Transcription Factor ◽

Acute Lymphoblastic Leukemia ◽

T Cell ◽

Lymphoblastic Leukemia ◽

Coding Region ◽

Eukaryotic Transcription ◽

Helix Loop Helix ◽

Putative Transcription Factor ◽

Cell Acute Lymphoblastic Leukemia ◽

Inappropriate Expression

Abstract The SCL gene, initially discovered at the site of a translocation breakpoint associated with the development of a stem cell leukemia, encodes a protein that contains the highly conserved basic helix-loop- helix (bHLH) motif found in a large array of eukaryotic transcription factors. Recently, we have described a nonrandom, site-specific SCL rearrangement in several T-cell acute lymphoblastic leukemia (ALL) cell lines that juxtaposes SCL with a distinct transcribed locus, SIL. The SIL/SCL rearrangement was found in leukemic blasts from 11 of 70 (16%) newly diagnosed T-cell ALL patients, a prevalence substantially higher than that of the t(11;14) translocation, which has previously been reported as the most frequent nonrandom chromosomal abnormality in T- cell ALL. We did not detect the SIL/SCL rearrangement in the leukemic blasts from 30 patients with B-cell precursor ALL, indicating that the rearrangement was specific for T-cell ALL. Analysis of RNA from these patients indicated that an SIL/SCL fusion mRNA was formed, joining SIL and SCL in a head-to-tail fashion. The fusion occurs in the 5′ untranslated region (UTR) of both genes, preserving the SCL coding region. The net result of this rearrangement is that SCL mRNA expression becomes regulated by the SIL promoter, leading to inappropriate SCL expression. The resultant inappropriate expression of this putative transcription factor may then contribute to leukemic transformation in T-cell ALL.

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