scholarly journals Mouse t-complex protein 11 is important for progressive motility in sperm†

2019 ◽  
Vol 102 (4) ◽  
pp. 852-862 ◽  
Author(s):  
Julio M Castaneda ◽  
Haruhiko Miyata ◽  
Denise R Archambeault ◽  
Yuhkoh Satouh ◽  
Zhifeng Yu ◽  
...  
Keyword(s):  
Chromosome 17 ◽  
Specific Gene ◽  
Sperm Function ◽  
Motile Sperm ◽  
Male Mice ◽  
Progressive Motility ◽  
T Complex ◽  
Naturally Occurring ◽  
Complex Protein ◽  
Kinase A

Abstract The t-complex is defined as naturally occurring variants of the proximal third of mouse chromosome 17 and has been studied by mouse geneticists for decades. This region contains many genes involved in processes from embryogenesis to sperm function. One such gene, t-complex protein 11 (Tcp11), was identified as a testis-specific gene whose protein is present in elongating spermatids. Later work on Tcp11 localized TCP11 to the sperm surface and acrosome cap and implicated TCP11 as important for sperm capacitation through the cyclic AMP/Protein Kinase A pathway. Here, we show that TCP11 is cytoplasmically localized to elongating spermatids and absent from sperm. In the absence of Tcp11, male mice have severely reduced fertility due to a significant decrease in progressively motile sperm; however, Tcp11-null sperm continues to undergo tyrosine phosphorylation, a hallmark of capacitation. Interestingly, null sperm displays reduced PKA activity, consistent with previous reports. Our work demonstrates that TCP11 functions in elongated spermatids to confer proper motility in mature sperm.

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 Distorter genes of the mouse t-complex impair male fertility when heterozygous

1987 ◽  
Vol 49 (1) ◽  
pp. 57-60 ◽  
Author(s):  
Mary F. Lyon
Keyword(s):  
Male Fertility ◽  
Genetic Background ◽  
Inbred Strains ◽  
Transmission Ratio Distortion ◽  
Chromosome 17 ◽  
Male Mice ◽  
Wild Type ◽  
T Complex ◽  
Ratio Distortion ◽  
Harmful Effects

SummaryMale mice heterozygous for two distorter genes, Tcd-1 and Tcd-2, of the mouse t-complex but homozygous wild type for the responder, were generated by crossing animals carrying the partial t-haplotypes th51 and th18 to inbred strains. The fertility of these males was then compared with that of their brothers carrying normal chromosome 17s. On three of the inbred backgrounds used, C3H/HeH, C57BL/6J and TFH/H, the th51th18 + / + + + males were significantly less fertile than their normal sibs. With the fourth inbred strain used, SM/JH, both types of male were nonnally fertile. This confirmed earlier preliminary findings that when both homologues of chromosome 17 carry wild-type alleles of the responder, heterozygosity for the distorter genes is sufficient to impair fertility, but the effect varies with genetic background. These results are consistent with the concept that both the transmission ratio distortion and the male sterility caused by the t-complex are due to harmful effects of the distorter genes on wild-type alleles of the responder.

scholarly journals Human t-Complex Protein 11 (TCP11), a Testis-Specific Gene Product, Is a Potential Determinant of the Sperm Morphology

2011 ◽  
Vol 224 (2) ◽  
pp. 111-117 ◽  
Author(s):  
Yanyan Liu ◽  
Min Jiang ◽  
Chao Li ◽  
Ping Yang ◽  
Huaqin Sun ◽  
...  
Keyword(s):  
Gene Product ◽  
Sperm Morphology ◽  
Specific Gene ◽  
T Complex ◽  
Complex Protein ◽  
Potential Determinant

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.

High-resolution mapping of sperm function defects in the t complex fourth inversion

1998 ◽  
Vol 9 (10) ◽  
pp. 825-830 ◽  
Author(s):  
A.A. Redkar ◽  
P. Olds-Clarke ◽  
L.M. Dugan ◽  
S.H. Pilder
Keyword(s):  
High Resolution ◽  
Sperm Function ◽  
T Complex ◽  
High Resolution Mapping ◽  
Resolution Mapping

Cloning of a Testis-Specific Gene Located Between Qa-2 and Upg-1 on Mouse Chromosome 17

H-2 Antigens ◽  
1987 ◽  
pp. 321-325
Author(s):  
Masanori Kasahara ◽  
Felipe Figueroa ◽  
Jan Klein
Keyword(s):  
Mouse Chromosome ◽  
Chromosome 17 ◽  
Specific Gene

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.

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