Plants have evolved intricate strategies to cope with various abiotic stresses. Ubiquitin-mediated protein degradation plays a key role in plant development as well as abiotic stress tolerance. In this study, we identify LAO1, an F-box protein with unknown function, as a negative regulator of plant fitness during nitrogen starvation. DOMINANT SUPPRESSOR OF KAR 2 (DSK2) interacts with and mediates the autophagic degradation of LAO1 protein during nitrogen starvation. The loss of LAO1 improves the fitness of an autophagy-deficient mutant, atg5-1, under nitrogen starvation. Intriguingly, mutations in DSK2 facilitate rather than reduce plant growth after nitrogen starvation. This unexpected effect of DSK2 knockout led us to discover that DSK2 also interacts with and degrades a group of class I TCP transcription factors. Phenotypic observations demonstrate that class I TCPs are crucial for plant adaptation to nitrogen starvation. Moreover, genetic analyses indicate that class I TCPs function downstream of LAO1 and counteract its negative effects. Collectively, our findings unveil a previously undescribed regulatory network governing plant fitness during nitrogen starvation.
Zhengke Zhang,Jialiang Liu,Donald J. Huber,Hongxia Qu,Ze Yun,Taotao Li,Yueming Jiang
Litchi fruit has high commercial value on the international market, but senesces rapidly after harvest. We used weighted gene co-expression network analysis (WGCNA) and degradome technology to investigate the molecular mechanisms of melatonin-mediated delay of litchi fruit senescence through application of exogenous melatonin and p-chlorophenylalanine (p-CPA, an inhibitor of melatonin biosynthesis) treatments. Results demonstrated that exogenous melatonin treatment delayed litchi fruit senescence while p-CPA accelerated senescence. Coupled analyses of transcriptome and physiological parameters of litchi fruit provided the correlation of network modules with dynamic changes in browning index during storage. Additionally, we found that microRNAs (miR858 and miR160a) and their targets were actively involved in melatonin-mediated delay of litchi fruit senescence. Melatonin treatment decreased abscisic acid (ABA) content but increased PP2C and F-box expression levels, suggesting the involvement of ABA signaling in melatonin-mediated antisenescence. The transcriptions of ZAT, NAC and DREB1 were activated by melatonin treatment. Moreover, the major functional genes involved in histone methylation, γ-aminobutyric acid (GABA) metabolism, energy production, reactive oxygen species (ROS) accumulation and cell death were identified in the melatonin-inhibited litchi pericarp browning. Taken together, we first constructed the global map of the important regulators and pathways to delay litchi senescence and pericarp browning mediated by melatonin.
危险品化学品经营许可证（带存储）