Light functions as the primary environmental stimulus and brassinosteroids (BRs) as important endogenous growth regulators throughout the plant lifecycle. Photomorphogenesis involves a series of vital developmental processes that require the suppression of BR-mediated seedling growth, but the mechanism underlying the light-controlled regulation of the BR pathway remains unclear. Here, we reveal that nuclear factor YC proteins (NF-YCs) function as essential repressors of the BR pathway during light-controlled hypocotyl growth in Arabidopsis thaliana. In the light, NF-YCs inhibit BR biosynthesis by directly targeting the promoter of the BR biosynthesis gene BR6ox2 and repressing its transcription. NF-YCs also interact with BIN2, a critical repressor of BR signaling, and facilitate its stabilization by promoting its Tyr200 autophosphorylation, thus inhibiting the BR signaling pathway. Consistently, loss-of-function mutants of NF-YCs show etiolated growth and constitutive BR responses, even in the light. Our findings uncover a dual role of NF-YCs in repressing BR biosynthesis and signaling, providing mechanistic insights into how light antagonizes the BR pathway to ensure photomorphogenic growth in Arabidopsis.

The MADS-box transcription factors are an ancient family of genes that regulate numerous physiological and biochemical processes in plants and facilitate the development of floral organs. However, the functions of most of these transcription factors in soybean remain unknown. In this work, a MADS-box gene, GmAGL1, was overexpressed in soybean. Phenotypic analysis showed that GmAGL1 overexpression not only resulted in early maturation but also promoted flowering and affected petal development. Furthermore, the GmAGL1 was much more effective at promoting flowering under long-day conditions than under short-day conditions. Transcriptome sequencing analysis showed that before flowering, the photoperiod pathway photoreceptor CRY2 and several circadian rhythm genes, such as SPA1, were significantly down-regulated, while some other flowering-promoting circadian genes, such as GI and LHY, and downstream genes related to flower development, such as FT, LEAFY, SEP1, SEP3, FUL, and AP1, were up-regulated compared with the control. Other genes related to the flowering pathway were not noticeably affected. The findings reported herein indicate that GmAGL1 may promote flowering mainly through the photoperiod pathway. Interestingly, while overexpression of GmAGL1 promoted plant maturity, no reduction in seed production or oil and protein contents was observed.

The primary cause for the limited shelf life of litchi fruit is rapid pericarp browning and decay. This study aims to evaluate the storability of 50 litchi varieties and establish a linear regression model for pericarp browning and decay based on 11 postharvest physical and chemical indices after 9 days of storage at room temperature. The results indicated that the average value of the browning index and decay rate significantly increased to 3.29% and 63.84% of 50 litchi varieties at day 9, respectively. Different litchi varieties showed different variations in appearance indicators, quality indicators, and physiological indicators. Furthermore, principal component analysis and cluster analysis revealed that Liu Li 2 Hao exhibited the highest resistance to storage, whereas Dong Long Mi Li, Jiao Pan Li, E Dan Li 2 Hao, and Ren Shan Li were not resistant. Stepwise multiple regression analysis further demonstrated that the factors were highly correlated with the decay index, with a partial correlation coefficient of 0.437 between the effective index and the decay index. Therefore, pericarp thickness, relative conductivity, pericarp laccase activity, and total soluble solids were significant indicators for the comprehensive evaluation of litchi browning and decay, and relative conductivity was the significant determinant causing fruit browning. These findings provide a new perspective on the sustainable development of the litchi industry.

Soybean mosaic virus (SMV) severely damages soybean [Glycine max (L.) Merr.] yield and seed quality. Moreover, the underlying genetic determinants of resistance to SMV remain largely unknown. Here, we performed a genome-wide association study (GWAS) of SMV resistance in a 219 panel across four environments and identified a new resistance-related gene, GmMLRK1, at the major resistance locus Rsv4 on chromosome 2. GmMLRK1 encodes a malectin-like receptor kinase (RK) that was induced earlier and to a greater degree in leaves of the SMV-resistant cultivar Kefeng No. 1 than in those of the susceptible cultivar Nannong 1138-2 after inoculation. We demonstrated that soybean plants overexpressing GmMLRK1 show broad-spectrum resistance to both strains SC7 and SC3 on the basis of the reduced viral accumulation and increased reactive oxygen species (ROS) production and local cell death associated with the hypersensitive response. In contrast, GmMLRK1 knockout (KO) mutants were more susceptible to both pathotypes. Haplotype analysis revealed the presence of five haplotypes (H1-H5) within the soybean population, and only H1 provided SMV resistance, which was independent of its tightly linked SMV resistance gene RNase-H at the same locus. These results▫highlight▫a novel gene that helps improve the understanding of SMV resistance and could be used for breeding resistant soybean accession.

Plants have evolved precise mechanisms to optimize immune responses against pathogens. ENHANCED DISEASE SUSCEPTIBILITY 1 (EDS1) plays a vital role in plant innate immunity by regulating basal resistance and effector-triggered immunity. Nucleocytoplasmic trafficking of EDS1 is required for resistance reinforcement, but the molecular mechanism remains elusive. Here, we show that EDS1-INTERACTING J PROTEIN1 (EIJ1), which acts as a DnaJ protein-like chaperone in response to pathogen infection, functions as an essential negative regulator of plant immunity by interacting with EDS1. The loss-of-function mutation of EIJ1 did not affect plant growth but significantly enhanced pathogen resistance. Upon pathogen infection, EIJ1 relocalized from the chloroplast to the cytoplasm, where it interacted with EDS1, thereby restricting pathogen-triggered trafficking of EDS1 to the nucleus and compromising resistance at an early infection stage. During disease development, EIJ1 was gradually degraded, allowing the nuclear accumulation of EDS1 for transcriptional resistance reinforcement. The avirulent strain Pst DC3000 (AvrRps4) abolished the repressive action of EIJ1 by rapidly inducing its degradation in the effector-triggered immunity response. Thus, our findings show that EIJ1 is an essential EDS1-dependent negative regulator of innate plant immunity and provide a mechanistic understanding of how the nuclear versus cytoplasmic distribution of EDS1 is regulated during the immune response.