OsGL6, a conserved AP2 domain protein, promotes leaf trichome initiation in rice.

Trichomes are specialized epidermal cells that play crucial roles in resisting environmental stress and enhancing plant development. In Arabidopsis thaliana, the main genes controlling trichome formation have been consecutively identified. However, few genes like this were reported in rice. In this study, we identified the hairy phenotype of indica variety 75-1-127. This was used to construct a segregation population with a cross of hairless variety Minghui63 (MH63) to fine map the trichome formation genes. Genetic analysis indicated that hairy phenotype was controlled by a pair of dominant genes on chromosome 6, which was designated as GLABRA6 (OsGL6). OsGL6 was an allele of HL6 gene whose sequences containing rich variations in genomes. Compared to wild type, the overexpressing transgenic lines revealed that OsGL6 promoted trichome initiation. We found that OsGL6 interacted with serine/threonine protein kinase OSK3 (OSK3) or COP9 signalosome complex subunit 5a (CSN5) in yeast. These results provide potential information for understanding the molecular mechanism of trichome formation in rice.

OsPRX2 contributes to stomatal closure and improves potassium deficiency tolerance in rice.

Peroxiredoxins (Prxs) which are thiol-based peroxidases have been implicated in the toxic reduction and intracellular concentration regulation of hydrogen peroxide. In Arabidopsis thaliana At2-CysPrxB (At5g06290) has been demonstrated to be essential in maintaining the water-water cycle for proper H2O2 scavenging. Although the mechanisms of 2-Cys Prxs have been extensively studied in Arabidopsis thaliana, the function of 2-Cys Prxs in rice is unclear. In this study, a rice homologue gene of At2-CysPrxB, OsPRX2 was investigated aiming to characterize the effect of 2-Cys Prxs on the K+-deficiency tolerance in rice. We found that OsPRX2 was localized in the chloroplast. Overexpressed OsPRX2 causes the stomatal closing and K+-deficiency tolerance increasing, while knockout of OsPRX2 lead to serious defects in leaves phenotype and the stomatal opening under the K+-deficiency tolerance. Detection of K+ accumulation, antioxidant activity of transgenic plants under the starvation of potassium, further confirmed that OsPRX2 is a potential target for engineering plants with improved potassium deficiency tolerance.

Roles of Hypothalamic-Pituitary-Adrenal Axis and Hypothalamus-Pituitary-Ovary Axis in the Abnormal Endocrine Functions in Patients with Polycystic Ovary Syndrome.

Polycystic ovary syndrome(PCOS) is a common reproductive endocrine disease in women of childbearing age. While it can be affected by a variety of factors,its pathophysiology remains unclear. Its clinical features mainly include anovulation,hyperandrogenism,and hyperinsulinemia,which are closely related with abnormal neuroendocrine system. Hypothalamic-pituitary-gonadal axis(HPG) plays a crucial regulatory role in various life activities in mammals. In particular,hypothalamic-pituitary-adrenal(HPA) axis and hypothalamus-pituitary-ovary(HPO) axis can be abnormal in PCOS patients. The corresponding abnormalities include abnormal gonadotropin releasing hormone pulse frequency,increased luteinizing hormone/follicle-stimulating hormone ratio,and excessive excretion of adrenal and ovarian androgens. Meanwhile,insulin and leptin also play key roles in endocrine dysfunction in PCOS patients. This article systematically reviews the role of HPA axis and HPO axis in the neuroendocrine dysfunction in PCOS patients.

Defective insulin signaling and the protective effects of dimethyldiguanide during follicular development in the ovaries of polycystic ovary syndrome.

It is established that the physiological effects of insulin are primarily mediated by the insulin signaling pathway. However, a defective insulin signaling is closely associated with the clinical manifestations of polycystic ovary syndrome (PCOS), which include excess androgen levels, insulin resistance and anovulation, and is involved in the pathophysiology of PCOS at the molecular level. Dimethyldiguanide (DMBG) has been widely employed to alleviate reproduction dysfunction in women with PCOS, however, the exact mechanism of this effect remains unclear. The objective of the present study was to investigate the effects of DMBG on the expression of the insulin signaling pathway in the ovaries of rats with PCOS, and to identify the potential underlying molecular mechanisms of these effects in PCOS. In the present study, a PCOS rat model was induced by letrozole, and successful establishment of the model was confirmed by examining ovarian histology and determining serum testosterone levels, by hematoxylin and eosin staining and ELISA, respectively. Subsequently, the expression of two key elements of insulin signaling, insulin receptor substrate (IRS)­2 and phosphatidylinositol 3­kinase (PI3K), was determined by immunohistochemistry and western blot analysis. The results demonstrated that IRS­2 and PI3K expression was markedly decreased in PCOS ovaries, which was rescued by DMBG treatment. These results indicate that IRS­2/PI3K signaling may be involved in the development of PCOS and the therapeutic effects of DMBG on PCOS. To further confirm the effects of DMBG on insulin signaling expression during this process, the expression of an additional two downstream proteins, phosphoinositide­dependent kinase­1 (PDK­1) and the mammalian target of rapamycin (mTOR), was also investigated in the present study, and the results demonstrated that the expression of PDK­1 and mTOR was significantly reduced in PCOS ovaries and increased following DMBG treatment, further indicating that altered insulin signaling may have an important role in the development and treatment of PCOS. In conclusion, the results of the present study indicate that the reduced expression of proteins involved in insulin signaling may contribute to the development of the clinical features of PCOS, and DMBG reverses reduced expression of insulin signaling components, by a mechanism that is yet to be determined, to attenuate certain symptoms of PCOS, such as obesity. To the best of our knowledge, the present study is the first to provide data regarding the detailed changes of insulin signaling during the development and treatment of PCOS, and may provide an important reference for clinical PCOS treatment.

Expression and clinical significance of the HIF-1a/ET-2 signaling pathway during the development and treatment of polycystic ovary syndrome.

Polycystic ovary syndrome (PCOS) is a major health problem in reproductive-aged women worldwide, but the precise pathogenesis of PCOS remains unclear. Our previous study revealed that hypoxia-inducible factor (HIF)-1a mediated endothelin (ET)-2 signaling plays an important role in ovulation in rats. Therefore, the present study used a PCOS rat model to test the hypotheses that HIF-1a signaling is expressed and inhibited in ovaries during PCOS formation and that the HIF-1a/ET-2 signaling pathway is a target of dimethyldiguanide (DMBG) in the clinical treatment of PCOS. First, the development of a PCOS model and the effect of DMBG treatment were examined through ovarian histology and serum hormone levels, which were consistent with previous reports. Second, HIF-1a and ET-2 expression were detected by immunohistochemistry and western blot. The results showed decreased HIF-1a/ET-2 expression in the ovaries of PCOS rats, whereas DMBG treatment reversed the protein decreases and improved the PCOS symptoms. Third, to understand the molecular mechanism, HIF-1a/ET-2 mRNA expression was also examined. Interestingly, HIF-1a mRNA increased in the ovaries of PCOS rats, while ET-2 mRNA decreased, indicating that HIF-1a protein degradation may be involved in POCS development and treatment. Finally, HIF prolyl hydroxylase (PHD) activity was examined to further clarify the contribution of HIF-1a signaling to the development and treatment of PCOS. The results suggested that the inhibition of HIF-1a/ET-2 signaling may be caused by increased PHD activity in PCOS. DMBG-treated PCOS may further activate HIF-1a signaling at least partly through inhibiting PHD activity. Taken together, these results indicate that HIF-1a signaling is inhibited in a PCOS rat model through increasing PHD activity. DMBG treatment improved PCOS by rescuing this pathway, suggesting that HIF-1a signaling plays an important role in the development and treatment of PCOS. This HIF-1a-mediated ET-2 signaling pathway may be an important mechanism regulating PCOS formation and treatment in mammalian ovaries in vivo and should be a new clinical target for PCOS prevention and treatment in the future.