Putative zinc finger protein encoded by a conserved chloroplast gene is very likely a subunit of a biotin-dependent carboxylase

1992 ◽  
Vol 20 (5) ◽  
pp. 759-761 ◽  
Author(s):  
Shyr-Jiann Li ◽  
John E. Cronan
Keyword(s):  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Chloroplast Gene ◽  
Finger Protein ◽  
A Subunit ◽  
Putative Zinc Finger

scholarly journals The putative zinc-finger protein WZF1 interacts with a cis-acting element of wheat histone genes

1993 ◽  
Vol 217 (3) ◽  
pp. 1049-1056 ◽  
Author(s):  
Ayako SAKAMOTO ◽  
Maki MINAMI ◽  
Gyung Hye HUH ◽  
Masaki IWABUCHI
Keyword(s):  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Histone Genes ◽  
Cis Acting ◽  
Finger Protein ◽  
Putative Zinc Finger

Gene Encoding a Putative Zinc Finger Protein inSynechocystisPCC6803

1991 ◽  
Vol 55 (9) ◽  
pp. 2259-2264
Author(s):  
Yutaka Ogura ◽  
Tadashi Yoshida ◽  
Yasukazu Nakamura ◽  
Miho Takemura ◽  
Kenji Oda ◽  
...  
Keyword(s):  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Gene Encoding ◽  
Finger Protein ◽  
Putative Zinc Finger

scholarly journals The yeast MOT2 gene encodes a putative zinc finger protein that serves as a global negative regulator affecting expression of several categories of genes, including mating-pheromone-responsive genes.

1994 ◽  
Vol 14 (5) ◽  
pp. 3150-3157 ◽  
Author(s):  
K Irie ◽  
K Yamaguchi ◽  
K Kawase ◽  
K Matsumoto
Keyword(s):  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Signal Transduction Pathway ◽  
Negative Regulator ◽  
Growth Defect ◽  
Recessive Mutation ◽  
Temperature Sensitive ◽  
Pheromone Response Pathway ◽  
Finger Protein ◽  
Putative Zinc Finger

The STE4 gene encodes the beta subunit of a heterotrimeric G protein that is an essential component of the pheromone signal transduction pathway. To identify downstream component(s) of Ste4, we sought pseudo-revertants that restored mating competence to ste4 mutants. The suppressor mot2 was isolated as a recessive mutation that restored conjugational competence to a temperature-sensitive ste4 mutant and simultaneously conferred a temperature-sensitive growth phenotype. The MOT2 gene encodes a putative zinc finger protein, the deletion of which resulted in temperature-sensitive growth, increased expression of FUS1 in the absence of pheromones, and suppression of a deletion of the alpha-factor receptor. On the other hand, sterility resulting from deletion of STE4 was not suppressed by the mot2 deletion. These phenotypes are similar to those associated with temperature-sensitive mutations in CDC36 and CDC39, which are proposed to encode general negative regulators of transcription rather than factors involved in the pheromone response pathway. Deletion of MOT2 also caused increased transcription of unrelated genes such as GAL7 and PHO84. Overexpression of MOT2 suppresses the growth defect of temperature-sensitive mutations in CDC36 and CDC39. These observations suggest that Mot2 functions as a general negative regulator of transcription in the same processes as Cdc36 and Cdc39.

scholarly journals Identification of a novel TGF-β-regulated gene encoding a putative zinc finger protein in human osteoblasts

1995 ◽  
Vol 23 (23) ◽  
pp. 4907-4912 ◽  
Author(s):  
Malayannan Subramaniam ◽  
Steven A. Harris ◽  
Merry Jo Oursler ◽  
Kay Rasmussen ◽  
B. Lawrence Riggs ◽  
...  
Keyword(s):  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Gene Encoding ◽  
Human Osteoblasts ◽  
Finger Protein ◽  
Putative Zinc Finger

Cloning and characterization of theCDZFPgene which encodes a putative zinc finger protein

DNA Sequence ◽  
2005 ◽  
Vol 16 (5) ◽  
pp. 391-396 ◽  
Author(s):  
Wenwen Tang ◽  
Jian Yuan ◽  
Xinya Chen ◽  
Yuxi Shan ◽  
Kuntian Luo ◽  
...  
Keyword(s):  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Finger Protein ◽  
Putative Zinc Finger

The yeast MOT2 gene encodes a putative zinc finger protein that serves as a global negative regulator affecting expression of several categories of genes, including mating-pheromone-responsive genes

1994 ◽  
Vol 14 (5) ◽  
pp. 3150-3157
Author(s):  
K Irie ◽  
K Yamaguchi ◽  
K Kawase ◽  
K Matsumoto
Keyword(s):  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Signal Transduction Pathway ◽  
Negative Regulator ◽  
Growth Defect ◽  
Recessive Mutation ◽  
Temperature Sensitive ◽  
Pheromone Response Pathway ◽  
Finger Protein ◽  
Putative Zinc Finger

The STE4 gene encodes the beta subunit of a heterotrimeric G protein that is an essential component of the pheromone signal transduction pathway. To identify downstream component(s) of Ste4, we sought pseudo-revertants that restored mating competence to ste4 mutants. The suppressor mot2 was isolated as a recessive mutation that restored conjugational competence to a temperature-sensitive ste4 mutant and simultaneously conferred a temperature-sensitive growth phenotype. The MOT2 gene encodes a putative zinc finger protein, the deletion of which resulted in temperature-sensitive growth, increased expression of FUS1 in the absence of pheromones, and suppression of a deletion of the alpha-factor receptor. On the other hand, sterility resulting from deletion of STE4 was not suppressed by the mot2 deletion. These phenotypes are similar to those associated with temperature-sensitive mutations in CDC36 and CDC39, which are proposed to encode general negative regulators of transcription rather than factors involved in the pheromone response pathway. Deletion of MOT2 also caused increased transcription of unrelated genes such as GAL7 and PHO84. Overexpression of MOT2 suppresses the growth defect of temperature-sensitive mutations in CDC36 and CDC39. These observations suggest that Mot2 functions as a general negative regulator of transcription in the same processes as Cdc36 and Cdc39.

scholarly journals Conidiophore Stalk-less1 Encodes a Putative Zinc-Finger Protein Involved in the Early Stage of Conidiation and Mycelial Infection in Magnaporthe oryzae

2009 ◽  
Vol 22 (4) ◽  
pp. 402-410 ◽  
Author(s):  
Zhuangzhi Zhou ◽  
Guihua Li ◽  
Chunhua Lin ◽  
Chaozu He
Keyword(s):  
Zinc Finger ◽  
Magnaporthe Oryzae ◽  
Wild Type Strain ◽  
Zinc Finger Protein ◽  
Early Stage ◽  
Host Cells ◽  
Rt Pcr ◽  
Finger Protein ◽  
Polymerase Chain ◽  
Putative Zinc Finger

Over recent decades, many pathogenicity genes of Magnaporthe oryzae have been identified but only a very limited number of genes have been identified that encode components of the conidiogenesis pathway. We report here a T-DNA insertional mutant that completely lost conidiation ability. Further investigation revealed that this mutant did not develop any conidiophore, and that the T-DNA was integrated into an annotated gene designated as conidiophore stalk-less1 or COS1. Complementation experiments suggested that COS1 may be a determinant of conidiation. Sequence analysis revealed that COS1 putatively encodes a 491-amino-acid zinc-finger protein and the protein was revealed localized to nucleus. Reverse-transcriptase polymerase chain reaction (RT-PCR)-based expression analysis indicated that two homologues of conidiophore-related genes were affected by the cos1 mutation, suggesting that Cos1 may function as a transcriptional regulator controlling genes responsible for conidiation. Inoculations of rice roots and wounded leaves with mycelia suggested that COS1 is not required for pathogenicity. Moreover, mutation of COS1 may aggravate infection of wounded leaves. Interestingly, different from the wild-type strain, mycelia of the cos1 mutant successfully infected host cells and caused visible symptoms on unwounded leaf blades and sheaths, indicating that Cos1 may have a role in some unknown mechanism of mycelial infection of M. oryzae.

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