scholarly journals Ssams2, a Gene Encoding GATA Transcription Factor, Is Required for Appressoria Formation and Chromosome Segregation in Sclerotinia sclerotiorum

2018 ◽  
Vol 9 ◽  
Author(s):  
Ling Liu ◽  
Qiaochu Wang ◽  
Xianghui Zhang ◽  
Jinliang Liu ◽  
Yanhua Zhang ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Sclerotinia Sclerotiorum ◽  
Chromosome Segregation ◽  
Gene Encoding ◽  
Gata Transcription Factor ◽  
Appressoria Formation

scholarly journals The Formaldehyde Dehydrogenase SsFdh1 Is Regulated by and Functionally Cooperates with the GATA Transcription Factor SsNsd1 in Sclerotinia sclerotiorum

mSystems ◽  
2019 ◽  
Vol 4 (5) ◽  
Author(s):  
Genglin Zhu ◽  
Gang Yu ◽  
Xianghui Zhang ◽  
Jinliang Liu ◽  
Yanhua Zhang ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Zinc Finger ◽  
Sclerotinia Sclerotiorum ◽  
Promoter Region ◽  
Nuclear Translocation ◽  
Effective Control ◽  
Formaldehyde Dehydrogenase ◽  
Content Type ◽  
Gata Transcription Factor ◽  
Gata Box

ABSTRACT GATA transcription factors (TFs) are common eukaryotic regulators, and glutathione-dependent formaldehyde dehydrogenases (GD-FDH) are ubiquitous enzymes with formaldehyde detoxification activity. In this study, the formaldehyde dehydrogenase Sclerotinia sclerotiorum Fdh1 (SsFdh1) was first characterized as an interacting partner of a GATA TF, SsNsd1, in S. sclerotiorum. Genetic analysis reveals that SsFdh1 functions in formaldehyde detoxification, nitrogen metabolism, sclerotium development, and pathogenicity. Both SsNsd1 and SsFdh1 harbor typical zinc finger motifs with conserved cysteine residues. SsNsd1 regulates SsFdh1 in two distinct manners. SsNsd1 directly binds to GATA-box DNA in the promoter region of Ssfdh1; SsNsd1 associates with SsFdh1 through disulfide bonds formed by conserved Cys residues. The SsNsd1-SsFdh1 interaction and nuclear translocation were found to prevent efficient binding of SsNsd1 to GATA-box DNA. Site-directed point mutation of these Cys residues influences the SsNsd1-SsFdh1 interaction and SsNsd1 DNA binding capacity. SsFdh1 is regulated by and functions jointly with the SsNsd1 factor, providing new insights into the complex transcriptional regulatory mechanisms of GATA factors. IMPORTANCE S. sclerotiorum is a pathogenic fungus with sclerotium and infection cushion development, making S. sclerotiorum one of the most challenging agricultural pathogens with no effective control method. We identified important sclerotium and compound appressorium formation determinants, SsNsd1 and SsFdh1, and investigated their regulatory mechanism at the molecular level. SsNsd1 and SsFdh1 are zinc finger motif-containing proteins and associate with each other in the nucleus. On other hand, SsNsd1, as a GATA transcription factor, directly binds to GATA-box DNA in the promoter region of Ssfdh1. The SsNsd1-SsFdh1 interaction and nuclear translocation were found to prevent efficient binding of SsNsd1 to GATA-box DNA. Our results provide insights into the role of the GATA transcription factor and its regulation of formaldehyde dehydrogenase in stress resistance, fungal sclerotium and compound appressorium development, and pathogenicity.

Tricho-Rhino-Phalangeal Syndrome with Supernumerary Teeth

2008 ◽  
Vol 87 (11) ◽  
pp. 1027-1031 ◽  
Author(s):  
P. Kantaputra ◽  
I. Miletich ◽  
H.-J. Lüdecke ◽  
E.Y. Suzuki ◽  
V. Praphanphoj ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Amino Acid ◽  
Zinc Finger ◽  
Clinical Features ◽  
Tooth Development ◽  
Supernumerary Teeth ◽  
Gene Encoding ◽  
Gata Transcription Factor ◽  
Craniofacial Defects

Tricho-rhino-phalangeal syndromes (TRPS) are caused by mutation or deletion of TRPS1, a gene encoding a GATA transcription factor. These disorders are characterized by abnormalities of the hair, face, and selected bones. Rare cases of individuals with TRPS displaying supernumerary teeth have been reported, but none of these has been examined molecularly. We used two different approaches to investigate a possible role of TRPS1 during tooth development. We looked at the expression of Tprs1 during mouse tooth development and analyzed the craniofacial defects of Trps1 mutant mice. In parallel, we investigated whether a 17-year-old Thai boy with clinical features of TRPS and 5 supernumerary teeth had mutation in TRPS1. We report here that Trps1 is expressed during mouse tooth development, and that an individual with TRPS with supernumerary teeth has the amino acid substitution A919V in the GATA zinc finger of TRPS1. These results suggest a role for TRPS1 in tooth morphogenesis.

scholarly journals SREB, a GATA Transcription Factor That Directs Disparate Fates in Blastomyces dermatitidis Including Morphogenesis and Siderophore Biosynthesis

2010 ◽  
Vol 6 (4) ◽  
pp. e1000846 ◽  
Author(s):  
Gregory M. Gauthier ◽  
Thomas D. Sullivan ◽  
Sergio S. Gallardo ◽  
T. Tristan Brandhorst ◽  
Amber J. Vanden Wymelenberg ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Blastomyces Dermatitidis ◽  
Siderophore Biosynthesis ◽  
Gata Transcription Factor

scholarly journals Differential activation mechanisms of two isoforms of Gcr1 transcription factor generated from spliced and un-spliced transcripts in Saccharomyces cerevisiae

2020 ◽  
Author(s):  
Seungwoo Cha ◽  
Chang Pyo Hong ◽  
Hyun Ah Kang ◽  
Ji-Sook Hahn
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Transcription Factor ◽  
Target Genes ◽  
Gene Encoding ◽  
Metabolic Switch ◽  
Differential Activation ◽  
N Terminus ◽  
Activation Mechanisms ◽  
In Trans ◽  
Separate Activation

Abstract Gcr1, an important transcription factor for glycolytic genes in Saccharomyces cerevisiae, was recently revealed to have two isoforms, Gcr1U and Gcr1S, produced from un-spliced and spliced transcripts, respectively. In this study, by generating strains expressing only Gcr1U or Gcr1S using the CRISPR/Cas9 system, we elucidate differential activation mechanisms of these two isoforms. The Gcr1U monomer forms an active complex with its coactivator Gcr2 homodimer, whereas Gcr1S acts as a homodimer without Gcr2. The USS domain, 55 residues at the N-terminus existing only in Gcr1U, inhibits dimerization of Gcr1U and even acts in trans to inhibit Gcr1S dimerization. The Gcr1S monomer inhibits the metabolic switch from fermentation to respiration by directly binding to the ALD4 promoter, which can be restored by overexpression of the ALD4 gene, encoding a mitochondrial aldehyde dehydrogenase required for ethanol utilization. Gcr1U and Gcr1S regulate almost the same target genes, but show unique activities depending on growth phase, suggesting that these isoforms play differential roles through separate activation mechanisms depending on environmental conditions.

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