Plants maintain a dynamic balance between growth and defense , and optimize allocation of resources for survival under constant pathogen infections. However, the underlying molecular regulatory mechanisms, especially in response to biotrophic bacterial infection, remain elusive. Here, we demonstrate that DELLA proteins and EDS1, an essential resistance regulator, form a central module modulating plant growth-defense tradeoffs via direct interaction. When infected by Pst DC3000, EDS1 rapidly promotes salicylic acid (SA) biosynthesis and resistance-related gene expression to prime defense response, while pathogen infection stabilizes DELLA proteins RGA and RGL3 to restrict growth in a partially EDS1-dependent manner, which facilitates plants to develop resistance to pathogens. However, the increasingly accumulated DELLAs interact with EDS1 to suppress SA overproduction and excessive resistance response. Taken together, our findings reveal a DELLA-EDS1-mediated feedback regulatory loop by which plants maintain the subtle balance between growth and defense to avoid excessive growth or defense in response to constant biotrophic pathogen attack.

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 remain 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.

Calcium-dependent protein kinases (CDPKs) play important roles in various aspects of plant physiology and involve in many cellular processes. However, genome-wide analysis of CDPK family in plant species is limited and few studies have been reported in soybean. In this study, a total of 39 genes encoding CDPKs were identified from the whole-genome sequence of soybean (Glycine max), which were denominated as GmCPK1-GmCPK39. These 39 CDPK genes could be classified into four subfamilies, and most genes showed tissue-specific expression patterns. Eight soybean CDPKs clustered together with the previously reported CDPKs related to pathogen, wounding, or herbivore stress were further analyzed. Differential gene expression analysis of these eight CDPK genes in response to herbivore and wounding stresses helps us identify GmCPK3 and GmCPK31 as the candidate genes for herbivore resistance in soybean, whose relative transcript abundance rapidly increased after wound and herbivore attacks. Sub-cellular localization revealed that GmCPK3 and GmCPK31 were localized in plasma membranes, which is consistent with previously reported plant defense related CDPKs. These results may suggest that GmCPK3 and GmCPK31 play important roles in the plant response to biotic stress. Simultaneously, our study will provide an important foundation for further functional characterization of the soybean CDPK gene family.

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BackgroundThe 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.ResultsIn 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.ConclusionsThe 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.Electronic supplementary materialThe online version of this article (10.1186/s12864-017-4402-2) contains supplementary material, which is available to authorized users.

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.

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