Tctex2: A Sperm Tail Surface Protein Mapping to the t-Complex

AbstractTransmission ratio distortion (TRD) in mouse t-haplotypes remains the most significant example of meiotic drive in vertebrates. While the underlying mechanism that fuels it is still mysterious, TRD is clearly a complex multigene phenomenon. The characterization of Tctex2 (t-complex testis expressed 2) shows it to be one of several candidates for involvement in TRD. Tctex2 maps to the t-complex and encodes a membrane-associated protein found exclusively on the sperm tail. The t-haplotype form of Tctex2 is aberrant in both the level of its expression and its primary amino acid sequence, but is nonetheless translated and transported to its normal location. The multiple amino acid changes in the t-form make it extremely unlikely that it can function normally and, since it is found on sperm tails, suggest that it may actively interfere with the development of normal gamete function in males. The possible role of Tctex2 in t -complex transmission ratio distortion and sterility is discussed

Molecular Identification of t(w5): Vps52 Promotes Pluripotential Cell Differentiation Through Cell-Cell Interactions

After implantation, pluripotent epiblasts are converted to embryonic ectoderm through cell-cell interactions that significantly change the transcriptional and epigenetic networks. An entree to understanding this vital developmental transition is the t(w5) mutation of the mouse t complex. This mutation produces highly specific defects in the embryonic ectoderm before gastrulation, leading to death of the embryonic ectoderm. Using a positional cloning approach, we have now identified the mutated gene, completing a decades-long search. The gene, vacuolar protein sorting 52 (Vps52), is a mouse homolog of yeast VPS52 that is involved in the retrograde trafficking of endosomes. Our data suggest that Vps52 acts in extraembryonic tissues to support the growth and differentiation of embryonic ectoderm via cell-cell interactions. It is also required in the formation of embryonic structures at a later stage of development, revealing hitherto unknown functions of Vps52 in the development of a multicellular organism.NSFCellular and Molecular Biolog

Genetic Change in Mutations at the T/t-Locus in the Mouse

Recessive lethal or semilethal alleles at the T/t locus in the mouse generate new t-variants, with characteristics different from the parent allele at a rate of about 10(-3). Almost invariably the variant chromosome carries marker genes derived from the opposite parental chromosome. New t-mutations obtained in this way are sometimes recessive lethals that are indistinguishable from those in already known complementation groups. Most derived t-mutations are viable, however. This paper summarizes data on the rate and types of variants produced by members of each of the six lethal complementation groups, and by semilethal alleles. It appears that particular complementation groups preferentially generate certain types of variants, and that in general, the pattern of variant production runs "uphill," that is, to less abnormal states. The data are compatible with the hypothesis that t-mutations represent some extent of altered chromosome and that variants are produced by loss of abnormal material

Surface Antigens Common to Mouse Cleavage Embryos and Primitive Teratocarcinoma Cells in Culture

Syngeneic antisera have been produced in mouse strain 129/Sv-CP males against the primitive cells of teratocarcinoma. These sera react specifically with the primitive cells and are negative on various types of differentiated teratoma cells derived from the same original tumor. They are negative on all other mouse cells tested, with the exception of male germ cells and cleavage-stage embryos. Thus, teratoma cells possess cell-surface antigens in common with normal cleavage-stage embryos