As sessile organisms, plants encounter a variety of environmental stresses and must optimize their growth for survival. Abscisic acid （ABA） and cytokinin antagonistically regulate many developmental processes and en...As sessile organisms, plants encounter a variety of environmental stresses and must optimize their growth for survival. Abscisic acid （ABA） and cytokinin antagonistically regulate many developmental processes and environmental stress responses in plants. However, the molecular mechanism underlying this antag- onism remains poorly defined. In this study, we demonstrated that Sucrose nonfermentingl-related kinases SnRK2.2, SnRK2.3, and SnRK2.6, the key kinases of the ABA signaling pathway, directly interact with and phosphorylate type-A response regulator 5 （ARR5）, a negative regulator of cytokinin signaling. The phosphorylation of ARR5 Ser residues by SnRK2s enhanced ARR5 protein stability. Accord- ingly, plants overexpressing ARR5 showed ABA hypersensitivity and drought tolerance, and these pheno- types could not be recapitulated by overexpressing a non-phosphorylated ARR5 mimic. Moreover, the type-B ARRs, ARR1, ARR11 and ARR12, physically interacted with SnRK2s and repressed the kinase activ- ity of SnRK2.6. The arrl, 11,12 triple mutant exhibited hypersensitivity to ABA. Genetic analysis demon- strated that SnRK2s act upstream of ARR5 but downstream of ARR1, ARR11 and ARR12 in mediating ABA response and drought tolerance. Taken together, this study unravels the antagonistic actions of several molecular components of the ABA and cytokinin signaling pathways in mediates drought stress response, providing significant insights into how plants coordinate growth and drought stress response by integrating multiple hormone pathways.展开更多
The uterotrophic assay has been commonly used to test environmental estrogens in vivo, however, it is often not sensitive enough sometimes. An alternative way is to evaluate estrogenicity through biomarker genes. Micr...The uterotrophic assay has been commonly used to test environmental estrogens in vivo, however, it is often not sensitive enough sometimes. An alternative way is to evaluate estrogenicity through biomarker genes. MicroRNA （miRNA） is a class of regulatory gene, which has been shown to be a good biomarker for many diseases and toxicological effects in recent years, and some evidences showed that estrogen induced response was partially mediated by miRNAs. In this study, two types of microarrays were used to test the 17[3-estradiol （E2） induced miRNA expression profile at different time points in the immature mouse uterus. Statistical analysis showed the aldehyde slide based array had less variation than the amino slide based array, and 11 dysregulated miRNAs were screened out for significant fold change. Real-time PCR was performed to further confirm that 4 out of 7 selected miRNAs, namely miR-451, miR-155, miR-335- 5p, and miR-365, are E2 regulated miRNAs in the uterus. The function of the predicted targets of these miRNAs is involved in cell grow control, which is consistent with the main E2 function in the uterus. MiR-451 had similar strong responses to E2 in the uterus of both immature and overiectomized mice, and could be a potential biomarker for estrogenicity in the uterus.展开更多
Many studies have focused on environmental estrogen-related diseases. However, no consistent gene markers or signatures for estrogenicity have been discovered in mammals. This study investigated the estrogenic effects...Many studies have focused on environmental estrogen-related diseases. However, no consistent gene markers or signatures for estrogenicity have been discovered in mammals. This study investigated the estrogenic effects of 17β-estradiol on the prostate in immature male mice. Consistent U-shaped responses were seen in bodyweight, ventral prostate epithelial morphology, and miRNA expression levels. Specifically, most estmdiol regulated miRNAs were downregulated at low doses of estradiol （0.2 and 2 μg. kg-1）, and whose expression returned to the control level at a larger dose （200 μg-kg-1）. The fi.mction of these regulated miRNAs is related to the prostate cancer and PI3K-Akt signaling pathways, which is consistent with the function of estmdiol. Furthermore, the miRNA-processing machinery, Drosha, in the prostate was also regulated in a similar pattern, which could be a part of the U-shaped miRNA expression mechanism. All of these data indicate that the prostate is a reliable organ for evaluating estrogenic activity and that the typical nonmonotonic dose-response relationship could be used as a novel biomarker for estrogenicity.展开更多
文摘As sessile organisms, plants encounter a variety of environmental stresses and must optimize their growth for survival. Abscisic acid （ABA） and cytokinin antagonistically regulate many developmental processes and environmental stress responses in plants. However, the molecular mechanism underlying this antag- onism remains poorly defined. In this study, we demonstrated that Sucrose nonfermentingl-related kinases SnRK2.2, SnRK2.3, and SnRK2.6, the key kinases of the ABA signaling pathway, directly interact with and phosphorylate type-A response regulator 5 （ARR5）, a negative regulator of cytokinin signaling. The phosphorylation of ARR5 Ser residues by SnRK2s enhanced ARR5 protein stability. Accord- ingly, plants overexpressing ARR5 showed ABA hypersensitivity and drought tolerance, and these pheno- types could not be recapitulated by overexpressing a non-phosphorylated ARR5 mimic. Moreover, the type-B ARRs, ARR1, ARR11 and ARR12, physically interacted with SnRK2s and repressed the kinase activ- ity of SnRK2.6. The arrl, 11,12 triple mutant exhibited hypersensitivity to ABA. Genetic analysis demon- strated that SnRK2s act upstream of ARR5 but downstream of ARR1, ARR11 and ARR12 in mediating ABA response and drought tolerance. Taken together, this study unravels the antagonistic actions of several molecular components of the ABA and cytokinin signaling pathways in mediates drought stress response, providing significant insights into how plants coordinate growth and drought stress response by integrating multiple hormone pathways.
文摘The uterotrophic assay has been commonly used to test environmental estrogens in vivo, however, it is often not sensitive enough sometimes. An alternative way is to evaluate estrogenicity through biomarker genes. MicroRNA （miRNA） is a class of regulatory gene, which has been shown to be a good biomarker for many diseases and toxicological effects in recent years, and some evidences showed that estrogen induced response was partially mediated by miRNAs. In this study, two types of microarrays were used to test the 17[3-estradiol （E2） induced miRNA expression profile at different time points in the immature mouse uterus. Statistical analysis showed the aldehyde slide based array had less variation than the amino slide based array, and 11 dysregulated miRNAs were screened out for significant fold change. Real-time PCR was performed to further confirm that 4 out of 7 selected miRNAs, namely miR-451, miR-155, miR-335- 5p, and miR-365, are E2 regulated miRNAs in the uterus. The function of the predicted targets of these miRNAs is involved in cell grow control, which is consistent with the main E2 function in the uterus. MiR-451 had similar strong responses to E2 in the uterus of both immature and overiectomized mice, and could be a potential biomarker for estrogenicity in the uterus.
基金Acknowledgements This work was financially supported by the National Natural Science Foundation of China （Grant Nos. 21377066 and 21007030）.
文摘Many studies have focused on environmental estrogen-related diseases. However, no consistent gene markers or signatures for estrogenicity have been discovered in mammals. This study investigated the estrogenic effects of 17β-estradiol on the prostate in immature male mice. Consistent U-shaped responses were seen in bodyweight, ventral prostate epithelial morphology, and miRNA expression levels. Specifically, most estmdiol regulated miRNAs were downregulated at low doses of estradiol （0.2 and 2 μg. kg-1）, and whose expression returned to the control level at a larger dose （200 μg-kg-1）. The fi.mction of these regulated miRNAs is related to the prostate cancer and PI3K-Akt signaling pathways, which is consistent with the function of estmdiol. Furthermore, the miRNA-processing machinery, Drosha, in the prostate was also regulated in a similar pattern, which could be a part of the U-shaped miRNA expression mechanism. All of these data indicate that the prostate is a reliable organ for evaluating estrogenic activity and that the typical nonmonotonic dose-response relationship could be used as a novel biomarker for estrogenicity.
