Leaf senescence is a complex developmental phase that involves both degenerative and nutrient recycling processes. It is characterized by loss of chlorophyll and the degradation of proteins, nucleic acids, lipids, and nutrient remobilization. The onset and progression of leaf senescence are controlled by an array of environmental cues (such as drought, darkness, extreme temperatures, and pathogen attack) and endogenous factors (including age, ethylene, jasmonic acid, salicylic acid, abscisic acid, and cytokinin). This review discusses the major breakthroughs in signal transduction during the onset of leaf senescence, in dark- and drought-mediated leaf senescence, and in various hormones regulating leaf senescence achieved in the past several years. Various signals show different mechanisms of controlling leaf senescence, and cross-talks between different signaling pathways make it more complex. Key senescence regulatory networks still need to be elucidated, including cross-talks and the interaction mechanisms of various environmental signals and internal factors.

If you are citing a reference for the first time in these legends, please include all new references in the Online Methods References section, and carry on the numbering from the main References section of the paper. Extended DataFig. 1 Alternative splicing site of the PHYC gene in xiaomi a, RNA-Seq reads of Jingu21. xiaomi genome sequences were used as reference genome. The blue vertical line shows the G-T mutation site. b, RNA-seq reads of xiaomi. The wrong splicing site was marked by a red arrow. Extended Data Fig. 2 Phenotypic and molecular characterization of the xiaomi-2 mutant a, Forty-day-old plants of Jingu21 (wild type, left) and xiaomi-2 (right) plants grown under natural long-day conditions. b, Heading date of Jingu21and xiaomi-2 under natural field conditions. The heading date of ≥ 20 plants was measured for each replicate (n = 3 biologically independent replicates, ≥ 102 in total). The bottom and top of boxes represent the first and third quartile, respectively. The middle line is the median and the whiskers represent the maximum and minimum values. Statistical analysis was performed using two-tailed Wilcoxon rank-sum test. c, A mature small-sized xiaomi-2 plant (right) compared to Jingu21 (left), at the 68th day in field. d, Plant height of Jingu21 and xiaomi-2 under natural field conditions. The plant height of ≥ 23 plants was measured for each replicate (n = 3 biologically independent replicates, ≥ 83 in total). e, Molecular charicterization of xiaomi-2. Exons and introns are denoted by filled boxes and lines, respectively. P2F and P2R represent a pair of primers used to amplify the fragments harboring the mutation site from the segregating M3 individuals (Primer sequences are listed in SupplementaryTable 3). c, Structure of PHYC and its mutation version deduced according to mutations in xiaomi-2. Scale bars, 10 cm in a and c. Extended Data Fig. 3 Sequence alignment of the GAF domain of PHYC in foxtail millet and its homologs software. Red box indicates the conserved residue Leu across all listed species that is substituted with His in xiaomi-2, demonstrating its functional importance for PHYC. Accession numbers for the aligned sequences: Arabidopsis thaliana NP_198433, Brachypodium distachyon XP_003559446, Brassica napus XP_013680236, Ipomoea nil XP_019162785, Oryza sativa AAF66603, Panicum miliaceum, RLN42126, Solanum lycopersicum NP_001307446, Sorghum bicolor XP_002466441, Triticum aestivum AAU06208, Vitis vinifera ACC6096 and Zea mays XP_008665426. PHYC protein in Jingu21 is presented as for Setaria italica (Si9G09200).Extended Data Fig. 4 Hi-C interaction matrices show the pairwise correlations between ordered scaffolds along the 9 pseudomolecules correlation. in T1 transgenic seeds as visualized for GFP expression or multiple (c) T-DNA insertions were scanned with a dissection microscope equipped with UV light. All experiments were performed for eight independent biological repeats, and similar results were obtained. Scale bars, 2 mm. Extended Data Fig. 6 PCR confirmation of the site-specif...

Leaf architecture directly determines canopy structure, and thus, grain yield in crops. Leaf droopiness is an agronomic trait primarily affecting the cereal leaf architecture but the genetic basis and underlying molecular mechanism of this trait remain unclear. Here, we report that DROOPY LEAF1 (DPY1), an LRR receptor-like kinase, plays a crucial role in determining leaf droopiness by controlling the brassinosteroid (BR) signaling output in Setaria, an emerging model for Panicoideae grasses. Loss-of-function mutation in DPY1 led to malformation of vascular sclerenchyma and low lignin content in leaves, and thus, an extremely droopy leaf phenotype, consistent with its preferential expression in leaf vascular tissues. DPY1 interacts with and competes for SiBAK1 and as a result, causes a sequential reduction in SiBRI1–SiBAK1 interaction, SiBRI1 phosphorylation, and downstream BR signaling. Conversely, DPY1 accumulation and affinity of the DPY1–SiBAK1 interaction are enhanced under BR treatment, thus preventing SiBRI1 from overactivation. As such, those findings reveal a negative feedback mechanism that represses leaf droopiness by preventing an overresponse of early BR signaling to excess BRs. Notably, plants overexpressing DPY1 have more upright leaves, thicker stems, and bigger panicles, suggesting potential utilization for yield improvement. The maize ortholog of DPY1 rescues the droopy leaves in dpy1, suggesting its conserved function in Panicoideae. Together, our study provides insights into how BR signaling is scrutinized by DPY1 to ensure the upward leaf architecture.