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Simple Summary: Liver receptor homolog-1 (LRH-1) is highly observed in tissues with secretory function, such as the ovaries, suggesting that LRH-1 may play an essential role in the ovarian endocrine. In particular, ovarian granulosa cells (GCs) are the functional cells that produce steroid hormones. The fate of GCs directly affects follicular development or atresia. These effects were lost in granulosa-specific LRH-1-knockout mice, showing that LRH-1 is a central modulator of ovarian function. However, the underlying mechanism LRH-1 in the bovine ovaries remains unclear. We aimed to detect the effect of LRH-1 on steroid hormones in bovine GCs and explore the potential relationship between LRH-1 and the fate of GCs. The results show that LRH-1 was specifically highly expressed in GCs of atretic follicles. Mechanistically, LRH-1 induced the apoptosis of bovine GCs by the progestogen receptor signaling pathway. While this finding provided new ideas for the study of follicular atresia, it also provided a theoretical basis for the clinical diagnosis and treatment for infertility in cow. The purpose of the present investigation was to assess the function of LRH-1 on GCs and the mechanisms involved. Here, LRH- was highly expressed in the bovine GCs of atretic follicles. Treatment with 50 μM of LRH-1 agonist (DLPC) significantly induced the expression of LRH-1 (p < 0.05). In particular, LRH-1 activation blocked the progestogen receptor signaling pathway via downregulating progesterone production and progestogen receptor levels (p < 0.05), but had no effect on 17 beta-estradiol synthesis. Meanwhile, LRH-1 activation promoted the apoptosis of GCs and increased the activity of caspase 3 (p < 0.05). Importantly, upregulating the progestogen receptor signaling pathway with progestogen could attenuate the LRH-1-induced proapoptotic effect. Moreover, treatment with progestogen decreased the activity of the proapoptotic gene caspase 3 and increased the expression of antiapoptotic gene Bcl2 in LRH-1 activated GCs (p < 0.05). Taken together, these results demonstrate that LRH-1 might be dependent on the progestogen receptor signaling pathway to modulate bovine follicular atresia. [ABSTRACT FROM AUTHOR]

In monocarpic plants, stem cells are fated to die. However, the potential mechanism of stem cell death has remained elusive. Here, we reveal that the levels of two forms of reactive oxygen species (ROS), superoxide anion free radical ( O 2 · − ) and hydrogen peroxide (H2O2), show dynamic changes in the shoot apex during the plant life cycle of Arabidopsis thaliana. We found that the level of O 2 · − decreased and disappeared at four weeks after bolting (WAB), while H2O2 appeared at 3 WAB and showed a burst at 5 WAB. The timing of dynamic changes in O 2 · − and H2O2 was delayed for approximately three weeks in clv3-2, which has a longer lifespan. Moreover, exogenous application of H2O2 inhibited the expression of the stem cell determinant WUSCHEL (WUS) and promoted the expression of the developmentally programmed cell death (dPCD) marker gene ORESARA 1 (ORE1). These results indicate that H2O2 triggers an important signal inducing dPCD in stem cells. Given that O 2 · − plays roles in maintaining WUS expression and stem cell activity, we speculate that the dynamic shift from O 2 · − to H2O2 in the shoot apex results in stem cell death. Our findings provide novel insights for understanding ROS-mediated regulation during plant stem cell death. [ABSTRACT FROM AUTHOR]