klumpfuss, a Drosophila gene encoding a member of the EGR family of transcription factors, is involved in bristle and leg development

Development ◽  
1997 ◽  
Vol 124 (16) ◽  
pp. 3123-3134 ◽  
Author(s):  
T. Klein ◽  
J.A. Campos-Ortega
Keyword(s):  
Transcription Factor ◽  
Zinc Finger ◽  
Wilms Tumor ◽  
Suppressor Gene ◽  
Transcription Unit ◽  
Gene Encoding ◽  
Zinc Finger Motifs ◽  
Leg Development ◽  
Putative Transcription Factor ◽  
Mother Cells

The klumpfuss (klu) transcription unit in Drosophila gives rise to two different transcripts of 4.5 and 4.9 kb, both of which encode a putative transcription factor with four zinc-finger motifs of the C2H2 class. Zinc-finger 2–4 are homologous to those of the proteins of the EGR transcription factor family. As in the case of the most divergent member of the family, the Wilms' tumor suppressor gene (WT-1), klu contains an additional zinc finger, which is only distantly related. Loss of klumpfuss function is semilethal and causes a variety of defects in bristles and legs of adults, as well as in mouth hooks and brains of larvae. Analysis of the mutants indicates that klumpfuss is required for proper specification and differentiation of a variety of cells, including the sensory organ mother cells and those of the distal parts of tarsal segments.

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 Gamma Radiation-Induced Damage in the Zinc Finger of the Transcription Factor IIIA

2016 ◽  
Vol 2016 ◽  
pp. 1-7 ◽  
Author(s):  
XiaoHong Zhang ◽  
YuJi Miao ◽  
XiaoDan Hu ◽  
Rui Min ◽  
PeiDang Liu ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Ionizing Radiation ◽  
Gamma Radiation ◽  
Zinc Finger ◽  
Cysteine Residues ◽  
Zinc Finger Motif ◽  
Thiol Groups ◽  
Transcription Factor Iiia ◽  
Zinc Finger Motifs ◽  
Radiation Induced

A zinc finger motif is an element of proteins that can specifically recognize and bind to DNA. Because they contain multiple cysteine residues, zinc finger motifs possess redox properties. Ionizing radiation generates a variety of free radicals in organisms. Zinc finger motifs, therefore, may be a target of ionizing radiation. The effect of gamma radiation on the zinc finger motifs in transcription factor IIIA (TFIIIA), a zinc finger protein, was investigated. TFIIIA was exposed to different gamma doses from 60Co sources. The dose rates were 0.20 Gy/min and 800 Gy/h, respectively. The binding capacity of zinc finger motifs in TFIIIA was determined using an electrophoretic mobility shift assay. We found that 1000 Gy of gamma radiation impaired the function of the zinc finger motifs in TFIIIA. The sites of radiation-induced damage in the zinc finger were the thiol groups of cysteine residues and zinc (II) ions. The thiol groups were oxidized to form disulfide bonds and the zinc (II) ions were indicated to be reduced to zinc atoms. These results indicate that the zinc finger motif is a target domain for gamma radiation, which may decrease 5S rRNA expression via impairment of the zinc finger motifs in TFIIIA.

scholarly journals Inhibition of red blood cell development by arsenic-induced disruption of GATA-1

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Xixi Zhou ◽  
Sebastian Medina ◽  
Alicia M. Bolt ◽  
Haikun Zhang ◽  
Guanghua Wan ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Zinc Finger ◽  
Zinc Fingers ◽  
Arsenic Exposure ◽  
In Vivo Studies ◽  
Regulatory Factor ◽  
Zinc Finger Motifs ◽  
First Time

Abstract Anemia is a hematological disorder that adversely affects the health of millions of people worldwide. Although many variables influence the development and exacerbation of anemia, one major contributing factor is the impairment of erythropoiesis. Normal erythropoiesis is highly regulated by the zinc finger transcription factor GATA-1. Disruption of the zinc finger motifs in GATA-1, such as produced by germline mutations, compromises the function of this critical transcription factor and causes dyserythropoietic anemia. Herein, we utilize a combination of in vitro and in vivo studies to provide evidence that arsenic, a widespread environmental toxicant, inhibits erythropoiesis likely through replacing zinc within the zinc fingers of the critical transcription factor GATA-1. We found that arsenic interacts with the N- and C-terminal zinc finger motifs of GATA-1, causing zinc loss and inhibition of DNA and protein binding activities, leading to dyserythropoiesis and an imbalance of hematopoietic differentiation. For the first time, we show that exposures to a prevalent environmental contaminant compromises the function of a key regulatory factor in erythropoiesis, producing effects functionally similar to inherited GATA-1 mutations. These findings highlight a novel molecular mechanism by which arsenic exposure may cause anemia and provide critical insights into potential prevention and intervention for arsenic-related anemias.

Analysis of expressed sequence tags in Brassica napus cotyledons damaged by crucifer flea beetle feeding

Genome ◽  
2012 ◽  
Vol 55 (2) ◽  
pp. 118-133 ◽  
Author(s):  
Margaret Gruber ◽  
Limin Wu ◽  
Matthew Links ◽  
Branimir Gjetvaj ◽  
Jonathan Durkin ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Brassica Napus ◽  
Zinc Finger ◽  
Unknown Function ◽  
Flea Beetle ◽  
Gene Families ◽  
Feeding Damage ◽  
Brassica Napus L ◽  
Gene Encoding ◽  
Crucifer Flea Beetle

The molecular basis of canola ( Brassica napus L.) susceptibility to the crucifer flea beetle (FB, Phyllotreta cruciferae Goeze) was investigated by comparing transcript representation in FB-damaged and undamaged cotyledons. The B. napus cotyledon transcriptome increased and diversified substantially after FB feeding damage. Twenty-two genes encoding proteins with unknown function, six encoding proteins involved in signaling, and a gene encoding a B-box zinc finger transcription factor were moderately or strongly changed in representation with FB feeding damage. Zinc finger and calcium-dependent genes formed the largest portion of transcription factors and signaling factors with changes in representation. Six genes with unknown function, one transcription factor, and one signaling gene specific to the FB-damaged library were co-represented in a FB-damaged leaf library. Out of 188 transcription factor and signaling gene families screened for “early” expression changes, 16 showed changes in expression within 8 h. Four of these early factors were zinc finger genes with representation only in the FB-damaged cotyledon. These genes are now available to test their potential at initiating or specifying cotyledon responses to crucifer FB feeding.

scholarly journals Identification of DNA Recognition Sequences and Protein Interaction Domains of the Multiple-Zn-Finger Protein Roaz

1998 ◽  
Vol 18 (11) ◽  
pp. 6447-6456 ◽  
Author(s):  
Robert Y. L. Tsai ◽  
Randall R. Reed
Keyword(s):  
Transcription Factor ◽  
Dna Binding ◽  
Binding Site ◽  
Zinc Finger ◽  
Protein Interaction ◽  
Inverted Repeat ◽  
Finger Protein ◽  
Zinc Finger Motifs ◽  
Half Site

ABSTRACT Roaz, a rat C2H2 zinc finger protein, plays a role in the regulation of olfactory neuronal differentiation through its interaction with the Olf-1/EBF transcription factor family. An additional role for the Roaz/Olf-1/EBF heterodimeric protein is suggested by its ability to regulate gene activation at a distinct promoter lacking Olf-1/EBF-binding sites. Using an in vitro binding-site selection assay (Selex), we demonstrate that Roaz protein binds to novel inverted perfect or imperfect repeats of GCACCC separated by 2 bp. We show that Roaz is capable of binding to a canonical consensus recognition sequence with high affinity (Kd = 3 nM). Analysis of the structural requirement for protein dimerization and DNA binding by Roaz reveals the role of specific zinc finger motifs in the Roaz protein for homodimerization and heterodimerization with the Olf-1/EBF transcription factor. The DNA-binding domain of Roaz is mapped to the N-terminal 277 amino acids, containing the first seven zinc finger motifs, which confers weak monomeric binding to a single half site and a stronger dimeric binding to the inverted repeat in a binding-site-dependent manner. Full-length protein can form dimers on both the inverted repeat and direct repeat but not on a single half site. These findings support the role of the TFIIIA-type Zn fingers in both protein-protein interaction and protein-DNA interaction and suggest distinct functions for specific motifs in proteins with a large number of zinc finger structures.

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