A Catalogue of Eukaryotic Transcription Factor Types, Their Evolutionary Origin, and Species Distribution

2011 ◽  
pp. 25-73 ◽  
Author(s):  
Matthew T. Weirauch ◽  
T.R. Hughes
Keyword(s):  
Transcription Factor ◽  
Species Distribution ◽  
Evolutionary Origin ◽  
Eukaryotic Transcription

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

Blood ◽  
1992 ◽  
Vol 79 (5) ◽  
pp. 1327-1333 ◽  
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.

scholarly journals TBP, a universal eukaryotic transcription factor?

1993 ◽  
Vol 7 (7b) ◽  
pp. 1291-1308 ◽  
Author(s):  
N Hernandez
Keyword(s):  
Transcription Factor ◽  
Eukaryotic Transcription

scholarly journals Prebending the estrogen response element destabilizes binding of the estrogen receptor DNA binding domain.

1997 ◽  
Vol 17 (6) ◽  
pp. 3173-3180 ◽  
Author(s):  
J Kim ◽  
G de Haan ◽  
A M Nardulli ◽  
D J Shapiro
Keyword(s):  
Estrogen Receptor ◽  
Transcription Factor ◽  
Dna Binding ◽  
Minor Groove ◽  
Dna Topology ◽  
Binding Domain ◽  
Dna Binding Domain ◽  
Eukaryotic Transcription ◽  
Estrogen Response ◽  
Direct Demonstration

Binding of many eukaryotic transcription regulatory proteins to their DNA recognition sequences results in conformational changes in DNA. To test the effect of altering DNA topology by prebending a transcription factor binding site, we examined the interaction of the estrogen receptor (ER) DNA binding domain (DBD) with prebent estrogen response elements (EREs). When the ERE in minicircle DNA was prebent toward the major groove, which is in the same direction as the ER-induced DNA bend, there was no significant effect on ER DBD binding relative to the linear counterparts. However, when the ERE was bent toward the minor groove, in a direction that opposes the ER-induced DNA bend, there was a four- to eightfold reduction in ER DBD binding. Since reduced binding was also observed with the ERE in nicked circles, the reduction in binding was not due to torsional force induced by binding of ER DBD to the prebent ERE in covalently closed minicircles. To determine the mechanism responsible for reduced binding to the prebent ERE, we examined the effect of prebending the ERE on the association and dissociation of the ER DBD. Binding of the ER DBD to ERE-containing minicircles was rapid when the EREs were prebent toward either the major or minor groove of the DNA (k(on) of 9.9 x 10(6) to 1.7 x 10(7) M(-1) s(-1)). Prebending the ERE toward the minor groove resulted in an increase in k(off) of four- to fivefold. Increased dissociation of the ER DBD from the ERE is, therefore, the major factor responsible for reduced binding of the ER DBD to an ERE prebent toward the minor groove. These data provide the first direct demonstration that the interaction of a eukaryotic transcription factor with its recognition sequence can be strongly influenced by altering DNA topology through prebending the DNA.

scholarly journals The Rice Bacterial Blight Resistance Gene xa5 Encodes a Novel Form of Disease Resistance

2004 ◽  
Vol 17 (12) ◽  
pp. 1348-1354 ◽  
Author(s):  
Anjali S. Iyer ◽  
Susan R. McCouch
Keyword(s):  
Transcription Factor ◽  
Disease Resistance ◽  
Resistance Gene ◽  
Bacterial Blight ◽  
Bacterial Blight Resistance ◽  
Nucleotide Substitutions ◽  
Gamma Subunit ◽  
Eukaryotic Transcription ◽  
Rice Bacterial Blight ◽  
Structural Classes

The rice xa5 gene for disease resistance to Xanthomonas oryzae pv. oryzae has been positionally cloned and encodes the gamma subunit of transcription factor IIA (TFIIAγ). TFIIAγ is a general eukaryotic transcription factor with no previously known role in disease resistance. xa5 is unusual in that it is recessive and does not conform to one of the typical resistance gene structural classes. Sequencing of TFIIAγ in resistant and susceptible isolines revealed two nucleotide substitutions resulting in an amino acid change between resistant and susceptible cultivars. This association was conserved across 27 resistant and nine susceptible rice lines in the Aus-Boro group.

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