Subhash C. Juneja

TL;DR: Targeted mutagenesis of connexin43 (Cx43) showed that its absence was compatible with survival of mouse embryos to term, even though mutant cell lines showed reduced dye coupling in vitro, which suggests that Cx43 plays an essential role in heart development but that there is functional compensation among connexins in other parts of the developing fetus.

TL;DR: It is shown that mutant mice with low levels of the spindle assembly checkpoint protein BubR1 develop progressive aneuploidy along with a variety of progeroid features, including short lifespan, cachectic dwarfism, lordokyphosis, cataracts, loss of subcutaneous fat and impaired wound healing.

TL;DR: In this paper, the expression of OB-Rb in human breast epithelial HBL100 cells and human breast carcinoma-derived T-47D cells was determined by anchorage-dependent and anchorageindependent growth assays.

TL;DR: The gonads of fetal and neonatal mice homozygous for a null mutation in the Gja1 gene encoding Cx43 were examined to determine whether the absence of this connexin has any consequences for gonadal development, and it was demonstrated that folliculogenesis can proceed to the primary (unilaminar) follicle stage in the absent of Cx 43 but that subsequent development is impaired.

TL;DR: It is reported that male mice with a null mutation in Hrb are infertile and display round-headed spermatozoa that lack an acrosome, concluding that Hrb is required for docking and/or fusion of proacrosomic vesicles during acrosomes biogenesis.