scholarly journals The testis-specific transcription factor TCFL5 responds to A MYB to elaborate the male meiotic program in placental mammals

2021 ◽  
Author(s):  
Deniz M. Ozata ◽  
Tianxiong Yu ◽  
Katharine Cecchini ◽  
Haiwei Mou ◽  
Amena Arif ◽  
...  
Keyword(s):  
Gene Expression ◽  
Transcription Factor ◽  
Rhesus Macaque ◽  
Pachytene Stage ◽  
Mrna Turnover ◽  
Male Mice ◽  
Late Pachytene ◽  
Specific Transcription Factor ◽  
Pachytene Spermatocytes

In male mice, the transcription factor (TF) A MYB initiates reprogramming of gene expression after spermatogonia enter meiosis. We report that A MYB activates Tcfl5, a testis-specific TF first produced in pachytene spermatocytes. Subsequently, A MYB and TCFL5 reciprocally reinforce their own transcription to establish an extensive circuit that regulates meiosis. TCFL5 promotes transcription of genes required for mRNA turnover, pachytene piRNA production, meiotic exit, and spermiogenesis. This transcriptional architecture is conserved in rhesus macaque, suggesting TCFL5 plays a central role in meiosis and spermiogenesis in placental mammals. Tcfl5em1/em1 mutants are sterile, and spermatogenesis arrests at the mid- or late-pachytene stage of meiosis.

scholarly journals Allele-specific transcription factor binding to common and rare variants associated with disease and gene expression

2016 ◽  
Vol 135 (5) ◽  
pp. 485-497 ◽  
Author(s):  
Marco Cavalli ◽  
Gang Pan ◽  
Helena Nord ◽  
Ola Wallerman ◽  
Emelie Wallén Arzt ◽  
...  
Keyword(s):  
Gene Expression ◽  
Transcription Factor ◽  
Rare Variants ◽  
Transcription Factor Binding ◽  
Specific Transcription Factor ◽  
Factor Binding ◽  
Allele Specific

scholarly journals Elf5 is a principal cell lineage specific transcription factor in the kidney that contributes to Aqp 2 and Avpr 2 gene expression

2017 ◽  
Vol 424 (1) ◽  
pp. 77-89 ◽  
Author(s):  
Justin Grassmeyer ◽  
Malini Mukherjee ◽  
Jennifer deRiso ◽  
Casey Hettinger ◽  
Monica Bailey ◽  
...  
Keyword(s):  
Gene Expression ◽  
Transcription Factor ◽  
Cell Lineage ◽  
Principal Cell ◽  
Specific Transcription Factor

Regulation of myogenin protein expression in denervated muscles from young and old rats

2000 ◽  
Vol 279 (1) ◽  
pp. R179-R188 ◽  
Author(s):  
Tatiana Y. Kostrominova ◽  
Peter C. D. Macpherson ◽  
Bruce M. Carlson ◽  
Daniel Goldman
Keyword(s):  
Gene Expression ◽  
Transcription Factor ◽  
Protein Expression ◽  
Rna Expression ◽  
Mrna Levels ◽  
Denervated Muscle ◽  
Α Subunit ◽  
Specific Transcription Factor ◽  
Old Rats ◽  
Denervated Muscles

Myogenin is a muscle-specific transcription factor participating in denervation-induced increases in nicotinic ACh receptor (nAChR) gene expression. Although myogenin RNA expression in denervated muscle is well documented, surprisingly little is known about myogenin protein expression. Therefore, we assayed myogenin protein and RNA in innervated and denervated muscles from young (4 mo) and old (24–32 mo) rats and compared this expression to that of the nAChR α-subunit RNA. These assays revealed increased myogenin protein expression within 1 day of denervation, preceding detectable increases in nAChR RNA. By 3 days of denervation, myogenin and nAChR α-subunit RNA were increased 500- and 130-fold, respectively, whereas myogenin protein increased 14-fold. Interestingly, old rats (32 mo) had 6-fold higher myogenin protein and ∼80-fold higher mRNA levels than young rats. However, after denervation, expression levels were similar for young and old animals. The increased myogenin expression during aging, which tends to localize to small fibers, likely reflects spontaneous denervation and/or regeneration. Our results show that increased myogenin protein in denervated muscles correlates with the upregulation of its mRNA.

scholarly journals Delta-thalassemia caused by disruption of the site for an erythroid- specific transcription factor, GATA-1, in the delta-globin gene promoter

Blood ◽  
1992 ◽  
Vol 80 (5) ◽  
pp. 1347-1351 ◽  
Author(s):  
M Matsuda ◽  
N Sakamoto ◽  
Y Fukumaki
Keyword(s):  
Gene Expression ◽  
Transcription Factor ◽  
Promoter Region ◽  
Globin Gene ◽  
Gene Promoter ◽  
Erythroid Cell ◽  
Specific Transcription Factor ◽  
Gel Retardation ◽  
Normal Individuals ◽  
Globin Gene Expression

Abstract Delta-thalassemia is a complex group of inherited disorders of globin genes characterized by impaired synthesis of the delta-globin chain. The T-C substitution was detected at position -77 of the delta-globin gene isolated from three independent Japanese individuals who were homozygotes for delta-thalassemia. To elucidate the significance of the mutation in delta-globin gene expression, we investigated the genotype of three delta-thalassemia homozygotes and 58 normal individuals using dot blot hybridization of the polymerase chain reaction (PCR)-amplified DNA. The mutation was observed in six alleles of three homozygotes, while no mutation was detected in 116 alleles of normal individuals, thereby indicating the close association of this mutation with the thalassemia phenotype. Since the mutation (TTATCT-TCATCT) is located within the inverted binding motif of GATA-1 (T or A-G-A-T-A-G or A), an erythroid cell-specific transcription factor, we did gel retardation assays using nuclear extracts from the erythroid cells. We found that GATA-1 binds the oligonucleotide spanning positions -61 to -90, but does not bind to the oligonucleotide with the mutation at position -77. Competition gel retardation assays showed that GATA-1 binding can be competed out by the fragment with the GATA-1 motif, but not with the mutant oligonucleotide. Analysis of the transient expression of the CAT gene linked to the delta-globin gene promoter region demonstrated that the construct with the mutant promoter region was expressed about 20- fold less compared with the normal one. Thus, the mutation at position - 77 impairs delta-globin gene expression by abolishing GATA-1 binding to the AGATAA sequence of the promoter region of the delta-globin gene. This provides a good example of involvement of tissue-specific transacting factors in the molecular pathogenesis of hereditary diseases.

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