Zfp-51, a murine zinc finger encoding gene mapping to the t-complex region of Chromosome 17, encodes 19 contiguous zinc fingers and is ubiquitously expressed

1994 ◽  
Vol 5 (6) ◽  
pp. 387-389 ◽  
Author(s):  
P. S. Burke ◽  
J. Don ◽  
D. J. Wolgemuth
Keyword(s):  
Gene Mapping ◽  
Zinc Finger ◽  
Zinc Fingers ◽  
Chromosome 17 ◽  
Complex Region ◽  
T Complex ◽  
Encoding Gene

scholarly journals Identification of a human ortholog of the mouse Dcpp gene locus, encoding a novel member of the CSP-1/Dcpp salivary protein family

2006 ◽  
Vol 28 (1) ◽  
pp. 129-140 ◽  
Author(s):  
John J. Mullins ◽  
Linda J. Mullins ◽  
Donald R. Dunbar ◽  
William J. Brammar ◽  
Kenneth W. Gross ◽  
...  
Keyword(s):  
Amino Acid ◽  
Oral Cavity ◽  
Salivary Glands ◽  
Mouse Chromosome ◽  
Mrna Translation ◽  
Salivary Protein ◽  
Protein Family ◽  
Chromosome 17 ◽  
Complex Region ◽  
T Complex

Salivary fluid, the collective product of numerous major and minor salivary glands, contains a range of secretory proteins that play key defensive, digestive, and gustatory roles in the oral cavity. To understand the distinct protein “signature” contributed by individual salivary glands to salivary secretions, we studied a family of proteins shown by in vitro mRNA translation to be abundantly expressed in mouse sublingual glands. Molecular cloning, Southern blotting, and restriction fragment length polymorphism analyses showed these to represent one known and two novel members of the common salivary protein (CSP-1)/Demilune cell and parotid protein (Dcpp) salivary protein family, the genes for which are closely linked in the T-complex region of mouse chromosome 17. Bioinformatic analysis identified a putative human CSP-1/Dcpp ortholog, HRPE773, expressed predominantly in human salivary tissue, that shows 31% amino acid identity and 45% amino acid similarity to the mouse Dcpp query sequence. The corresponding human gene displays a similar structure to the mouse Dcpp genes and is located on human chromosome 16 in a region known to be syntenic with the T-complex region of mouse chromosome 17. The predicted mouse and human proteins both display classical NH2-terminal signal sequences, putative jacalin-related lectin domains, and potential N-linked glycosylation sites, suggesting secretion via sublingual saliva into the oral cavity where they may display antimicrobial activity or provide a defensive coating to enamel. Identification of a human CSP-1/Dcpp ortholog therefore provides a key tool for investigation of salivary protein function in human oral health and disease.

Genetic mapping of 10 microsatellites in the t complex region of mouse Chromosome 17

1998 ◽  
Vol 9 (6) ◽  
pp. 472-472 ◽  
Author(s):  
Corine Vernet ◽  
Kuniya Abe ◽  
Karen Artzt
Keyword(s):  
Genetic Mapping ◽  
Mouse Chromosome ◽  
Chromosome 17 ◽  
Complex Region ◽  
T Complex

Gene mapping within the T/t complex of the mouse. III: t-lethal genes are arranged in three clusters on chromosome 17

Cell ◽  
1984 ◽  
Vol 39 (3) ◽  
pp. 565-572 ◽  
Author(s):  
Karen Artzt
Keyword(s):  
Gene Mapping ◽  
Chromosome 17 ◽  
T Complex ◽  
Lethal Genes

scholarly journals A Haplolethal Locus Uncovered by Deletions in the Mouse t Complex

Genetics ◽  
2002 ◽  
Vol 160 (2) ◽  
pp. 675-682
Author(s):  
Victoria L Browning ◽  
Rebecca A Bergstrom ◽  
Sandra Daigle ◽  
John C Schimenti
Keyword(s):  
Gene Dosage ◽  
Es Cells ◽  
Embryonic Stem ◽  
Chromosome 17 ◽  
Mammalian Development ◽  
T Complex ◽  
Segmental Aneuploidy ◽  
Systematic Exploration ◽  
Radiation Induced ◽  
Altered Gene

Abstract Proper levels of gene expression are important for normal mammalian development. Typically, altered gene dosage caused by karyotypic abnormalities results in embryonic lethality or birth defects. Segmental aneuploidy can be compatible with life but often results in contiguous gene syndromes. The ability to manipulate the mouse genome allows the systematic exploration of regions that are affected by alterations in gene dosage. To explore the effects of segmental haploidy in the mouse t complex on chromosome 17, radiation-induced deletion complexes centered at the Sod2 and D17Leh94 loci were generated in embryonic stem (ES) cells. A small interval was identified that, when hemizygous, caused specific embryonic lethal phenotypes (exencephaly and edema) in most fetuses. The penetrance of these phenotypes was background dependent. Additionally, evidence for parent-of-origin effects was observed. This genetic approach should be useful for identifying genes that are imprinted or whose dosage is critical for normal embryonic development.

Only two of the five zinc fingers of the eukaryotic transcriptional repressor PRDI-BF1 are required for sequence-specific DNA binding

1992 ◽  
Vol 12 (5) ◽  
pp. 1940-1949
Author(s):  
A D Keller ◽  
T Maniatis
Keyword(s):  
Dna Binding ◽  
Zinc Finger ◽  
Specific Binding ◽  
Regulatory Element ◽  
Zinc Fingers ◽  
Transcriptional Repressor ◽  
Gene Promoter ◽  
Binding Activity ◽  
Necessary And Sufficient ◽  
Sequence Requirements

The eukaryotic transcriptional repressor PRDI-BF1 contains five zinc fingers of the C2H2 type, and the protein binds specifically to PRDI, a 14-bp regulatory element of the beta interferon gene promoter. We have investigated the amino acid sequence requirements for specific binding to PRDI and found that the five zinc fingers and a short stretch of amino acids N terminal to the first finger are necessary and sufficient for PRDI-specific binding. The contribution of individual zinc fingers to DNA binding was investigated by inserting them in various combinations into another zinc finger-containing DNA-binding protein whose own fingers had been removed. We found that insertion of PRDI-BF1 zinc fingers 1 and 2 confer PRDI-binding activity on the recipient protein. In contrast, the insertion of PRDI-BF1 zinc fingers 2 through 5, the insertion of zinc finger 1 or 2 alone, and the insertion of zinc fingers 1 and 2 in reverse order did not confer PRDI-binding activity. We conclude that the first two PRDI-BF1 zinc fingers together are sufficient for the sequence-specific recognition of PRDI.

Molecular Studies of Mouse Chromosome 17 and the T Complex

1984 ◽  
pp. 141-156 ◽  
Author(s):  
Lee M. Silver ◽  
James I. Garrels ◽  
Hans Lehrach
Keyword(s):  
Mouse Chromosome ◽  
Chromosome 17 ◽  
T Complex ◽  
Molecular Studies

scholarly journals Functional analysis of mutations of murine chromosome 17 with the use of tertiary trisomy.

Genetics ◽  
1991 ◽  
Vol 127 (4) ◽  
pp. 781-788
Author(s):  
A Ruvinsky ◽  
A Agulnik ◽  
S Agulnik ◽  
M Rogachova
Keyword(s):  
Functional Analysis ◽  
Gene Dosage ◽  
Tail Length ◽  
Proximal Region ◽  
The Other ◽  
Chromosome 17 ◽  
Recessive Mutations ◽  
T Complex ◽  
Functional Nature ◽  
Morphogenetic Effects

Abstract Analysis of the functional nature of mutations can be based on comparisons of their manifestation in organisms with a deletion or duplication of a particular chromosome segment. With the use of reciprocal translocation T(16;17)43H, it is feasible to produce mice with tertiary trisomy of the proximal region of chromosome 17. The mutations on chromosome 17 we tested included brachyury (T), hairpin tail (Thp), kinky (Fuki), quaking (qk), tufted (tf), as well as tct (t complex tail interaction), and tcl (t complex lethal) that are specific to t haplotypes. The set of dominant and recessive mutations was assigned to two groups: one obligatory, manifesting itself in the phenotype independently of the number of normal alleles in di- and trisomics, and the other facultative, phenotypically manifesting itself depending upon the dosage of mutant alleles. A model was derived from analysis of the interaction of the T and Thp mutations with t haplotypes. It seeks to explain the morphogenetic effects of the mutations observed in mice of different genotypes. The tir gene is postulated to reside on chromosome 17 within its framework. It is suggested that the gene dosage ratio at the tir and tct loci determines tail length.

scholarly journals Genetic and molecular analysis of the proximal region of the mouse t-complex using new molecular probes and partial t-haplotypes.

Genetics ◽  
1990 ◽  
Vol 126 (4) ◽  
pp. 1103-1114 ◽  
Author(s):  
C A Howard ◽  
G R Gummere ◽  
M F Lyon ◽  
D Bennett ◽  
K Artzt
Keyword(s):  
Wild Mouse ◽  
Molecular Probes ◽  
Proximal Region ◽  
Chromosome 17 ◽  
Lethal Gene ◽  
Strong Linkage Disequilibrium ◽  
Wild Type ◽  
T Complex ◽  
Naturally Occurring ◽  
Normal Transmission

Abstract The t-complex is located on the proximal third of chromosome 17 in the house mouse. Naturally occurring variant forms of the t-complex, known as complete t-haplotypes, are found in wild mouse populations. The t-haplotypes contain at least four nonoverlapping inversions that suppress recombination with the wild-type chromosome, and lock into strong linkage disequilibrium loci affecting normal transmission of the chromosome, male gametogenesis and embryonic development. Partial t-haplotypes derived through rare recombination between t-haplotypes and wild-type homologs have been critical in the analysis of these properties. Utilizing two new DNA probes. Au3 and Au9, and several previously described probes, we have analyzed the genetic structure of several partial t-haplotypes that have arisen in our laboratory, as well as several wild-type chromosomes deleted for loci in this region. With this approach we have been able to further our understanding of the structural and dynamic characteristics of the proximal region of the t-complex. Specifically, we have localized the D17Tul locus as most proximal known in t-haplotypes, achieved a better structural analysis of the partial t-haplotype t6, and defined the structure and lethal gene content of partial t-haplotypes derived from the lethal tw73 haplotype.

scholarly journals Evolutionary Analysis of the Zinc Finger and Homeoboxes Family of Proteins Identifies Multiple Conserved Domains and a Common Early Chordate Ancestor

2020 ◽  
Vol 12 (3) ◽  
pp. 174-184
Author(s):  
Alexandra N Nail ◽  
Jeramiah J Smith ◽  
Martha L Peterson ◽  
Brett T Spear
Keyword(s):  
Zinc Finger ◽  
Cultured Cells ◽  
Zinc Fingers ◽  
Evolutionary Analysis ◽  
Vertebrate Lineage ◽  
Amino Terminal ◽  
Small Family ◽  
Sea Squirt ◽  
Wide Range ◽  
Carboxy Terminal

Abstract The Zinc Fingers and Homeoboxes (Zhx) proteins, Zhx1, Zhx2, and Zhx3, comprise a small family of proteins containing two amino-terminal C2–H2 zinc fingers and four or five carboxy-terminal homeodomains. These multiple homeodomains make Zhx proteins unusual because the majority of homeodomain-containing proteins contain a single homeodomain. Studies in cultured cells and mice suggest that Zhx proteins can function as positive or negative transcriptional regulators. Zhx2 regulates numerous hepatic genes, and all three Zhx proteins have been implicated in different cancers. Because Zhx proteins contain multiple predicted homeodomains, are associated with interesting physiological traits, and seem to be only present in the vertebrate lineage, we investigated the evolutionary history of this small family by comparing Zhx homologs from a wide range of chordates. This analysis indicates that the zinc finger motifs and homeodomains are highly similar among all Zhx proteins and also identifies additional Zhx-specific conserved regions, including a 13 amino acid amino-terminal motif that is nearly identical among all gnathostome Zhx proteins. We found single Zhx proteins in the sea lamprey (Petromyzon marinus) and in the nonvertebrate chordates sea squirt (Ciona intestinalis) and lancelet (Branchiostoma floridae); these Zhx proteins are most similar to gnathostome Zhx3. Based on our analyses, we propose that a duplication of the primordial Zhx gene gave rise to Zhx3 and the precursor to Zhx1 and Zhx2. A subsequent tandem duplication of this precursor generated Zhx1 and Zhx2 found in gnathostomes.

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