氮(N)是限制植物生长的关键元素,氮沉降增加已成为影响草原土壤-植物养分循环的重要驱动因素。然而,不同添加速率和频率对土壤-植物化学计量关系的影响机制仍不明确。本研究基于温带典型草原长期氮添加试验,设计3种氮添加速率[0、10、20...氮(N)是限制植物生长的关键元素,氮沉降增加已成为影响草原土壤-植物养分循环的重要驱动因素。然而,不同添加速率和频率对土壤-植物化学计量关系的影响机制仍不明确。本研究基于温带典型草原长期氮添加试验,设计3种氮添加速率[0、10、20 g N/(m^(2)·a)]和2种氮添加频率(一年2次和12次),研究表层土壤化学计量特征以及优势植物羊草和大针茅的碳(C)、N、磷(P)含量及其与生物量之间的关系。结果表明,氮添加显著提高土壤C、N含量并降低P含量,导致土壤C∶N下降、C∶P和N∶P升高。在高频率添加条件下,20 g N/(m^(2)·a)处理的土壤P含量降幅以及C∶P、N∶P的增幅均低于10 g N/(m^(2)·a)处理。此外,氮添加速率增加了植物N含量,降低了P含量,使植物C∶N降低,N∶P和C∶P升高;而氮添加频率对植物和土壤养分及其化学计量比均未表现出显著影响。路径分析表明,氮添加速率通过改变土壤和植物养分含量间接调控植物化学计量比,进而促进2种优势植物的地上和地下生物量增加,而氮添加频率无显著影响。本研究表明氮添加驱动植物由N限制向N饱和转变,并进一步加剧P限制,可能成为限制草原生态系统生产力提升的关键过程。展开更多
Activation of spinal cord neural stem cells(NSCs)and subsequent neurogenesis holds a promising alternative for spinal cord injury(SCI)repair.Our previous study demonstrated that complement C3a,derived from reactive as...Activation of spinal cord neural stem cells(NSCs)and subsequent neurogenesis holds a promising alternative for spinal cord injury(SCI)repair.Our previous study demonstrated that complement C3a,derived from reactive astrocytes,inhibits NSC proliferation by suppressing protein aggregate clearance through the deubiquitinating enzyme ubiquitin carboxy-terminal hydrolase L1(UCHL1)-proteasome system post-SCI.However,the potential molecular mechanism by which C3a modulates NSC activation via this pathway remains unclear.Here,we revealed that C3a/C3a receptor(C3aR)signaling activated NF-κB p65,which in turn inhibited Nrf2 activity and UCHL1 expression,resulting in diminished proteasome activity and the accumulation of protein aggregates,and ultimately impaired NSC activation.Both knockdown of NF-κB p65 and Nrf2 upregulation restored UCHL1 expression and proteasome activity in vitro,promoting NSC activation by enhancing protein aggregate clearance.Mechanistically,we found that NF-κB p65 regulated Nrf2 activity through a dual mechanism:(1)promoting Keap1-dependent ubiquitination and proteasome degradation of Nrf2;(2)inhibiting protein kinase C-mediated Nrf2 phosphorylation and nuclear translocation.Using the dual-luciferase reporter assay and chromatin immunoprecipitation(ChIP)analysis,we further identified UCHL1 as a direct transcriptional target of Nrf2.Importantly,in vivo experiments using SCI mice confirmed that either C3aR blockade,NF-κB p65 knockdown,or Nrf2 overexpression could rescue SCI-induced UCHL1 downregulation.Together,this study uncovers the C3a-NF-κB p65-Nrf2-UCHL1-proteasome axis as a critical regulator of NSC activation after SCI.This may provide novel molecular targets and intervention strategies for SCI repair.展开更多
文摘氮(N)是限制植物生长的关键元素,氮沉降增加已成为影响草原土壤-植物养分循环的重要驱动因素。然而,不同添加速率和频率对土壤-植物化学计量关系的影响机制仍不明确。本研究基于温带典型草原长期氮添加试验,设计3种氮添加速率[0、10、20 g N/(m^(2)·a)]和2种氮添加频率(一年2次和12次),研究表层土壤化学计量特征以及优势植物羊草和大针茅的碳(C)、N、磷(P)含量及其与生物量之间的关系。结果表明,氮添加显著提高土壤C、N含量并降低P含量,导致土壤C∶N下降、C∶P和N∶P升高。在高频率添加条件下,20 g N/(m^(2)·a)处理的土壤P含量降幅以及C∶P、N∶P的增幅均低于10 g N/(m^(2)·a)处理。此外,氮添加速率增加了植物N含量,降低了P含量,使植物C∶N降低,N∶P和C∶P升高;而氮添加频率对植物和土壤养分及其化学计量比均未表现出显著影响。路径分析表明,氮添加速率通过改变土壤和植物养分含量间接调控植物化学计量比,进而促进2种优势植物的地上和地下生物量增加,而氮添加频率无显著影响。本研究表明氮添加驱动植物由N限制向N饱和转变,并进一步加剧P限制,可能成为限制草原生态系统生产力提升的关键过程。
基金supported by the National Natural Science Foundation of China(82071362 and 82270669)Key Project of the Regional Joint Fund of Guangdong Province(2023B1515120077)+3 种基金Basic Research Program of Shenzhen Science and Technology Innovation Commission(JCYJ20210324123001003 and JCYJ20220530144801003)Shenzhen Key Laboratory of Bone Tissue Repair and Translational Research(ZDSYS20230626091402006)the Innovation and Entrepreneurship Training Program for College Students,Sun Yat-sen University(20242150)the Leading Innovation and Entrepreneurship Team Program of Zhejiang Province,China(2023R01005).
文摘Activation of spinal cord neural stem cells(NSCs)and subsequent neurogenesis holds a promising alternative for spinal cord injury(SCI)repair.Our previous study demonstrated that complement C3a,derived from reactive astrocytes,inhibits NSC proliferation by suppressing protein aggregate clearance through the deubiquitinating enzyme ubiquitin carboxy-terminal hydrolase L1(UCHL1)-proteasome system post-SCI.However,the potential molecular mechanism by which C3a modulates NSC activation via this pathway remains unclear.Here,we revealed that C3a/C3a receptor(C3aR)signaling activated NF-κB p65,which in turn inhibited Nrf2 activity and UCHL1 expression,resulting in diminished proteasome activity and the accumulation of protein aggregates,and ultimately impaired NSC activation.Both knockdown of NF-κB p65 and Nrf2 upregulation restored UCHL1 expression and proteasome activity in vitro,promoting NSC activation by enhancing protein aggregate clearance.Mechanistically,we found that NF-κB p65 regulated Nrf2 activity through a dual mechanism:(1)promoting Keap1-dependent ubiquitination and proteasome degradation of Nrf2;(2)inhibiting protein kinase C-mediated Nrf2 phosphorylation and nuclear translocation.Using the dual-luciferase reporter assay and chromatin immunoprecipitation(ChIP)analysis,we further identified UCHL1 as a direct transcriptional target of Nrf2.Importantly,in vivo experiments using SCI mice confirmed that either C3aR blockade,NF-κB p65 knockdown,or Nrf2 overexpression could rescue SCI-induced UCHL1 downregulation.Together,this study uncovers the C3a-NF-κB p65-Nrf2-UCHL1-proteasome axis as a critical regulator of NSC activation after SCI.This may provide novel molecular targets and intervention strategies for SCI repair.
