Phytochrome-interacting factors(PIFs)have been established as negative regulators of vascular patterning and xylem differentiation in the herbaceous plant Arabidopsis thaliana,however,the regulatory role of PIFs in se...Phytochrome-interacting factors(PIFs)have been established as negative regulators of vascular patterning and xylem differentiation in the herbaceous plant Arabidopsis thaliana,however,the regulatory role of PIFs in secondary growth in woody species remains unclear.Here,we examines the expression patterns and involvement of PtoPIF3.1 and PtoPIF3.2 during stem growth and secondary xylem development in Populus tomentosa.Overexpression of either PtoPIF3.1 or PtoPIF3.2 significantly enhances both longitudinal stem growth and radial wood development.Conversely,Ptopif3.1 and Ptopif3.2 mutants generated by CRISPR-mediated genome editing exhibit reciprocal phenotypic defects.Exogenous auxin application partially restores the phenotypes of Ptopif3.1 and Ptopif3.2 mutants,and the auxin biosynthesis-deficient mutant Ptoyuc8 exhibits developmental abnormalities similar to those observed in Ptopif3 mutants.Further analysis reveal that PtoPIF3s directly bind to and activate expression of PtoYUC8 and cell expansion-related genes PtoEXPA1.1/1.2,while modulating cambial division and expression of secondary xylem development marker genes(PtoWOX4,PtoANT,PtoCYCD3s,and PtoHB7/8)through auxin-mediated signaling.Together,our findings establish PtoPIF3.1/3.2 as key regulators that coordinate stem elongation and secondary growth in Populus,highlighting the functional divergence of PIF homologs between herbaceous and woody species.展开更多
Background:Human skin is affected by ultraviolet rays on a daily basis,and excessive ultraviolet radiation(UVR)can lead to sunburn erythema,tanning,photoaging,and skin tumors.The combination of Astragali Radix(AR)and ...Background:Human skin is affected by ultraviolet rays on a daily basis,and excessive ultraviolet radiation(UVR)can lead to sunburn erythema,tanning,photoaging,and skin tumors.The combination of Astragali Radix(AR)and Anemarrhenae Rhizoma(AAR)is a common pairing in traditional Chinese medicine(TCM).According to earlier studies,they possess properties capable of alleviating the adverse impacts of UVR on the skin.However,the specific actions and underlying mechanisms require further investigation.The study aims to analyze the efficacy of AR-AAR in preventing UVR-induced skin damage and to clarify the associated molecular mechanisms.Methods:Potential signaling pathways by which AR and AAR may protect against UVR-induced skin damage were identified with network pharmacology,molecular docking techniques and molecular dynamics(MD)simulation.Except the normal group,the back skin of SD rats was exposed to 1.1 mW/cm^(2) UVA combined with 0.1 mW/cm^(2) UVB daily,and the UVR skin damage model was established.Morphological features of skin tissues of different groups were discovered through Hematoxylin and Eosin(HE)staining,Masson staining,Weigert staining.ELISA was utilized to measure the levels of reactive oxygen species(ROS),Interleukin 6(IL-6),Interleukin 1β(IL-1β)and Tumor necrosis factos-α(TNF-α)in skin tissues.RT-PCR and Western blot were employed to quantify the mRNA and protein contents of PI3K,AKT,and MMP-9.Results:Network pharmacology analysis predicts that AR-AAR may improve skin damage induced by UVR through the PI3K/AKT signaling pathway.Histological staining shows that AR-AAR can significantly reduce inflammatory infiltration and fibrosis in damaged skin.Treatment with AR-AAR(2:1)significantly reduced the expression levels of IL-1β,IL-6,TNF-αand ROS in UVR-damaged rat skin.After treatment with AR-AAR(2:1),not only did the relative mRNA expression levels of PI3K and AKT and the protein expression levels of PI3K,AKT,P-PI3K,and P-AKT increase,but the mRNA and protein expression levels of MMP-9 decreased.Conclusion:The study indicate that the AR-AAR combination and its active components may mitigate UVR skin damage by modulating the PI3K/AKT signaling pathway.展开更多
基金upported by grants from the National Key Research and Development Program of China(2022YFD1201600)the National Natural Science Foundation of China(32371903).
文摘Phytochrome-interacting factors(PIFs)have been established as negative regulators of vascular patterning and xylem differentiation in the herbaceous plant Arabidopsis thaliana,however,the regulatory role of PIFs in secondary growth in woody species remains unclear.Here,we examines the expression patterns and involvement of PtoPIF3.1 and PtoPIF3.2 during stem growth and secondary xylem development in Populus tomentosa.Overexpression of either PtoPIF3.1 or PtoPIF3.2 significantly enhances both longitudinal stem growth and radial wood development.Conversely,Ptopif3.1 and Ptopif3.2 mutants generated by CRISPR-mediated genome editing exhibit reciprocal phenotypic defects.Exogenous auxin application partially restores the phenotypes of Ptopif3.1 and Ptopif3.2 mutants,and the auxin biosynthesis-deficient mutant Ptoyuc8 exhibits developmental abnormalities similar to those observed in Ptopif3 mutants.Further analysis reveal that PtoPIF3s directly bind to and activate expression of PtoYUC8 and cell expansion-related genes PtoEXPA1.1/1.2,while modulating cambial division and expression of secondary xylem development marker genes(PtoWOX4,PtoANT,PtoCYCD3s,and PtoHB7/8)through auxin-mediated signaling.Together,our findings establish PtoPIF3.1/3.2 as key regulators that coordinate stem elongation and secondary growth in Populus,highlighting the functional divergence of PIF homologs between herbaceous and woody species.
基金supported by the Shaanxi Qinchuang Yuan“scientist+engineer”team construction(No.2023KXJ-080)Shaanxi Chiral Drug Engineering Technology Research Center(Department of Science and Technology of Shaanxi Province.No.[2011]-251).
文摘Background:Human skin is affected by ultraviolet rays on a daily basis,and excessive ultraviolet radiation(UVR)can lead to sunburn erythema,tanning,photoaging,and skin tumors.The combination of Astragali Radix(AR)and Anemarrhenae Rhizoma(AAR)is a common pairing in traditional Chinese medicine(TCM).According to earlier studies,they possess properties capable of alleviating the adverse impacts of UVR on the skin.However,the specific actions and underlying mechanisms require further investigation.The study aims to analyze the efficacy of AR-AAR in preventing UVR-induced skin damage and to clarify the associated molecular mechanisms.Methods:Potential signaling pathways by which AR and AAR may protect against UVR-induced skin damage were identified with network pharmacology,molecular docking techniques and molecular dynamics(MD)simulation.Except the normal group,the back skin of SD rats was exposed to 1.1 mW/cm^(2) UVA combined with 0.1 mW/cm^(2) UVB daily,and the UVR skin damage model was established.Morphological features of skin tissues of different groups were discovered through Hematoxylin and Eosin(HE)staining,Masson staining,Weigert staining.ELISA was utilized to measure the levels of reactive oxygen species(ROS),Interleukin 6(IL-6),Interleukin 1β(IL-1β)and Tumor necrosis factos-α(TNF-α)in skin tissues.RT-PCR and Western blot were employed to quantify the mRNA and protein contents of PI3K,AKT,and MMP-9.Results:Network pharmacology analysis predicts that AR-AAR may improve skin damage induced by UVR through the PI3K/AKT signaling pathway.Histological staining shows that AR-AAR can significantly reduce inflammatory infiltration and fibrosis in damaged skin.Treatment with AR-AAR(2:1)significantly reduced the expression levels of IL-1β,IL-6,TNF-αand ROS in UVR-damaged rat skin.After treatment with AR-AAR(2:1),not only did the relative mRNA expression levels of PI3K and AKT and the protein expression levels of PI3K,AKT,P-PI3K,and P-AKT increase,but the mRNA and protein expression levels of MMP-9 decreased.Conclusion:The study indicate that the AR-AAR combination and its active components may mitigate UVR skin damage by modulating the PI3K/AKT signaling pathway.
