甜樱桃是世界最受欢迎的水果之一。早先，我们发现了一种黑色暗格真菌S16，它能够促进樱桃砧木吉塞拉5号的生长。然而，关于它们之间作用的分子机制还不甚了解。在本次研究中，我们分析了与S16共生的樱桃根部的生理指标以及转录组本，初步阐释了S16促樱桃生长的分子机制。与S16共生后，樱桃幼苗的活力更强。而且，与对照相比，S16共生根部共鉴定到4249个差异表达基因。这些基因涉及到与植物代谢、激素相关的生长过程。而且，与氮调控相关的基因高度富集。生理指标测定表明，S16能够促进樱桃幼苗利用NO₃^-转运蛋白来吸收氮源。因此，此次RNA测序数据库可以更加深入了从分子机制层面解析黑色暗格真菌促樱桃的生长过程。

Recent reports have demonstrated that follicular atresia is initiated or caused by granulosa cell apoptosis followed by theca cell degeneration in mammalian ovaries, but the mechanism of follicular atresia is still to be elucidated. Therefore, our present study was designed to examine our hypothesis that the changes of follicular microenvironment induce the granulosa cell apoptosis during pocrine follicular atresia in vivo. We firstly isolated intact porcine antral follicles and identified them into three groups, healthy follicles (HF), early atretic follicles (EAF) and progressed atretic follicles (PAF) through morphology and histology. To further confirm their status, we detected hormone levels in follicular fluids and the expression level of apoptosis gene Bax in granulosa cells. The rate of progesterone (P) and estradiol (E2) was increased with the expression of Bax, indicating hormone can be used as a marker of granulosa cell apoptosis or follicular atresia. Finally, we analyzed the expression level of hormone receptor genes in granulosa cells and their relationship with follicular atresia. In PAF, the expression of Progesterone receptor (PGR) was increased significantly while estradiol receptor (ER) had no notable changes, which suggesting the increased-PGR accelerated the effect of P-stimulated granulosa cell apoptosis. The dramatic increasing of androgen receptor (AR) expression in PAF and the obvious increase of tumor necrosis factor-α receptor (TNFR) in EAF indicated that there are different pathways regulating granulosa cell apoptosis during follicular atresia. Together, our results suggested that different pathways of granulosa cell apoptosis was induced by changing the follicular microenvironment during follicular atresia.