Disease relevance of t

• Male sterility of the mouse t-complex is due to homozygosity of the distorter genes [1].
• Importantly, the model predicts that the mechanism of hybrid sterility associated with the t-complex is the same as the mechanism of intraspecific homozygous sterility [2].
• We have previously demonstrated that a mouse t-complex-associated antigen (ESGp) is present on the cell surface, specifically at areas of cell-cell contact, of cleavage stage embryos and embryonal carcinoma cell lines [3].
• Relationships between a human homologue of the mouse t-complex, epilepsy, and birth defects have yet to be proven [4].
• Observations on autoimmune orchitis in sterile mice carrying a recessive lethal mutation at the T/t complex exhibiting spontaneous allergic orchitis [5].

Psychiatry related information on t

• The region is equivalent to part of the mouse t complex and could be of relevance to human development [6].

High impact information on t

• The t complex-encoded GTPase-activating protein Tagap1 acts as a transmission ratio distorter in mice [7].
• The mouse t complex responder (Tcr) locus plays a central haploid-specific role in the transmission ratio distortion phenotype expressed during germ cell differentiation in t-carrying males [8].
• A large inverted duplication allows homologous recombination between chromosomes heterozygous for the proximal t complex inversion [9].
• We have cloned the gene for an abundant testicular germ cell protein, t complex polypeptide 1, which has a variant form in t haplotypes, TCP-1A [10].
• Molecular cloning and sequence analysis of a haploid expressed gene encoding t complex polypeptide 1 [10].

Biological context of t

• The t complex spans 20 cM of the proximal region of mouse chromosome 17 [11].
• Partial haplotypes derived through rare recombination between a t haplotype and its wild-type homolog have been essential in the genetic analysis of these various properties of the t complex [12].
• The t complex on chromosome 17 of the house mouse is an exceptional model for studying the genetic control of transmission ratio, gametogenesis, and embryogenesis [12].
• Physical mapping of male fertility and meiotic drive quantitative trait loci in the mouse t complex using chromosome deficiencies [11].
• For simplicity all t-complex lethal genes properly named tcl-tx are shortened to tx [13].

Anatomical context of t

• A mutation in T2 disrupts notochord development, pointing to the existence of a second T/t complex gene involved in axis development [14].
• The discovery of a protein, p63/6.9, that is synthesized by both somatic and germ cells and coded for by a gene, Tcp-1, within the t complex provides a molecular probe for examining transmission ratio distortion in t mice [15].
• To determine whether p63/6.9 is a direct gene product of the T/t complex, testicular cytoplasmic RNA from mice bearing the genotypes +/+, +/t and t/t was translated in a rabbit reticulocyte-derived cell-free system, and translated products were analyzed by two-dimensional gel electrophoresis [16].
• Several mouse mutants in the distal region of the mouse t-complex affecting blastocyst and embryonic ectoderm formation also map to this region [17].
• Molecular analysis of a 19,000-Mr protein from the Chlamydomonas flagellum reveals that it is homologous to the t complex-encoded protein Tctex-2, which is a candidate for one of the distorter products that cause the extreme transmission ratio distortion (meiotic drive) of the murine t complex [18].

Associations of t with chemical compounds

• Previously we described an embryonic cell surface glycoprotein, ESGp, associated with the t-embryonic lethal alleles of the mouse t complex [19].
• The t-complex-encoded guanine nucleotide exchange factor Fgd2 reveals that two opposing signaling pathways promote transmission ratio distortion in the mouse [20].
• TCP-11, the product of a t-complex gene, is the putative receptor for FPP: Fab fragments of anti-TCP-11 antibodies have the same effect as FPP on mouse spermatozoa and Gln-FPP, a competitive inhibitor of FPP, also competitively inhibits responses to the Fab fragments [21].

Physical interactions of t

• Chromosome 17 of the mouse carries the H-2 complex and the T/t complex [22].

Regulatory relationships of t

• These genes were named t-complex testis-expressed (Tctex) genes [23].

Other interactions of t

• To overcome limitations imposed by recombination suppression, we used a series of deletions within the t complex in trans to t chromosomes to characterize the Tcd1 region [11].
• Thus, Hst-6 provides direct access to the molecular basis of t haplotype-specific alterations in sperm function that emanate from the t complex distal inversion [24].
• A quantitative variant of glyoxalase-1 associated with the t-complex in house mice is described [25].
• An H-2K gene of the tw32 mutant at the T/t complex is a close parent of an H-2Kq gene [26].
• In previous studies, a locus responsible for hybrid sterility in the genus Mus,Hst-4, was mapped to the distal inversion of the t complex on chromosome 17 [24].

Analytical, diagnostic and therapeutic context of t

• Gene mapping within the T/t complex of the mouse. IV: The inverted MHC is intermingled with several t-lethal genes [27].
• In a study of 26 tumors, genotyped by Southern blot analysis of the major histocompatibility complex (MHC), we measured the distance between the centromere and the start of the t-complex as 5.6 +/- 2.3 cM [28].
• Extent of the mouse t complex and its inversions shown by in situ hybridization [29].
• The cis-trans test shows no evidence for a functional relationship between two mouse t complex lethal mutations: implications for the evolution of t haplotypes [30].
• A group of cosmid clones was isolated from the region of the mouse t complex and analysed by a rapid restriction mapping protocol based on linearization of circular cosmid DNA in vitro [31].

References