花生病害严重威胁花生生产，而通过种间杂交创制抗病材料是解决这一问题的有效途径。本研究利用花生栽培品种四粒红与野生种Arachis duranensis杂交，通过胚拯救和组织培养获得了种间杂种F₁幼苗，细胞学和分子标记鉴定表明种间杂种F₁为真杂种。进一步对扩繁F1幼苗进行秋水仙素处理，获得了F₁种子，命名为Am1210。通过寡核苷酸荧光原位杂交鉴定、分子标记鉴定、表型鉴定和网斑病鉴定，我们发现：1）Am1210是Slh和ZW55种间杂交异源六倍体花生；2）蔓生、单粒或二粒荚果和红色种皮等性状相对于直立型、多粒荚果和褐色种皮为显性性状；3）Am1210的网斑病抗性与Slh相比显著提高，表明这种抗性来自于A. duranensis。此外，本研究还开发了69个显性和共显性分子标记，可用于种间杂种鉴定及未来A. duranensis染色体片段易位或渗入系的鉴定。

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.