Background:The mechanism of gene regulation by the H2A deubiquitinase BAP1 is unclear. Results: BAP1 loss increases FoxK2 target gene expression but not in the absence of the H2A ubiquitin ligase complex Ring1B-Bmi1. Conclusion: BAP1 counteracts Ring1B-Bmi1-dependent activation of FoxK2 target genes. Significance: BAP1 deficiency in cancer cells might cause up-regulation of target genes in a Ring1B-Bmi1-dependent manner.
Fowl sperm motility was measured by altering the extracellular pH (pHe) at 30 degrees C and 40 degrees C. At 30 degrees C, the motility of intact spermatozoa was vigorous in a medium in the wide pHe range of 7.3-10.1. In contrast, intact spermatozoa were almost immotile at 40 degrees C in medium below a pHe of 8.1. However, the motility could be restored by increasing the pHe; maximum motility was obtained in medium at pHe 9.4. Stimulation of the motility of demembranated spermatozoa at 40 degrees C was also observed with an increased pHe. However, demembranated spermatozoa at 40 degrees C that had been stimulated by increasing the pHe lost their motility when 1 mmol CaCl2 l-1 was added. Motility was restored by the subsequent addition of 2 mmol EGTA l-1. At a high pHe at 40 degrees C, the flagellar ATPase activity of crude dynein extract was not affected, regardless of the addition of CaCl2 or EGTA. The intracellular pH (pHi) of intact spermatozoa, estimated by measuring the accumulation of 9-aminoacridine fluorescence, increased with increasing pHe at both 30 degrees C and 40 degrees C. These results demonstrate that the reversible temperature-dependent immobilization of fowl spermatozoa at 40 degrees C is inhibited by an increased pHi. Furthermore, it is possible that the effects of the increased pHi may not act directly on dynein ATPase activity, but are mediated by a Ca(2+)-related substance(s) on the axoneme.
In this paper, we clarify the relationship between myoblast orientation and my ogene sis by pattering myoblasts and analyzing gene expression of self-assembling muscle tissue over time. Previous studies have shown that it is possible to pattern muscle cells by culturing cells on chemically or physically patterned surfaces. We applied this technique to uncover the how the physical placement of cells and mechanobiological adhesive surface sensing influence intercellular communication and intracellular dynamics resulting in the different form and functionality of the final muscle tissue. By using microchannels with different widths, we controlled the cell fusion directions and successfully fabricated muscle tissue with different orientation distributions. Furthermore, we analyzed mRNA expression and protein synthesis known to play a key role in myogenesis and revealed that the maturation speed accelerates by patterning myoblasts and the optimal channel width was estimated about 100 �m.
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