Genomic decoding of breeding history to guide breeding-by-design in rice.

Deciphering the intrinsic molecular logic of empirical crop breeding from a genomic perspective is a decisive prerequisite for breeding-by-design (BbD), but remains not well established. Here, we decoded the historical features of past rice breeding by phenotyping and haplotyping 546 accessions covering the majority of cultivars bred in the history of Northeast China (NEC). We revealed that three groups founded the genetic diversities in NEC rice with distinct evolution patterns and traced and verified the breeding footprints to known or genome-wide association study (GWAS)-detected quantitative trait loci (QTLs), or introgressions from indica sub-species with chronological changes in allele frequencies. Then we summarized a rice breeding trend/principle in NEC, and combined with the successful example in breeding and application of Zhongkefa5 to demonstrate the guiding value of our conclusion for BbD in practice. Our study provides a paradigm for decoding the breeding history of a specific crop to guide BbD, which may have implications in different crop breeding.

An activated form of NB-ARC protein RLS1 functions with cysteine-rich receptor-like protein RMC to trigger cell death in rice.

A key event that follows pathogen recognition by a resistance (R) protein containing an NB-ARC (nucleotide-binding adaptor shared by Apaf-1, R proteins, and Ced-4) domain is hypersensitive response (HR)-type cell death accompanied by accumulation of reactive oxygen species and nitric oxide. However, the integral mechanisms that underlie this process remain relatively opaque. Here, we show that a gain-of-function mutation in the NB-ARC protein RLS1 (Rapid Leaf Senescence 1) triggers high-light-dependent HR-like cell death in rice. The RLS1-mediated defense response is largely independent of salicylic acid accumulation, NPR1 (Nonexpressor of Pathogenesis-Related Gene 1) activity, and RAR1 (Required for Mla12 Resistance 1) function. A screen for suppressors of RLS1 activation identified RMC (Root Meander Curling) as essential for the RLS1-activated defense response. RMC encodes a cysteine-rich receptor-like secreted protein (CRRSP) and functions as an RLS1-binding partner. Intriguingly, their co-expression resulted in a change in the pattern of subcellular localization and was sufficient to trigger cell death accompanied by a decrease in the activity of the antioxidant enzyme APX1. Collectively, our findings reveal an NB-ARC-CRRSP signaling module that modulates oxidative state, the cell death process, and associated immunity responses in rice.

Synergistic interplay of ABA and BR signal in regulating plant growth and adaptation.

Complex antagonistic interactions between abscisic acid (ABA) and brassinosteroid (BR) signalling pathways have been widely documented. However, whether or how ABA interacts synergistically with BR in plants remains to be elucidated. Here, we report that low, but not high, concentration of ABA increases lamina joint inclination of rice seedling, which requires functional BR biosynthesis and signalling. Transcriptome analyses confirm that about 60% of low-concentration ABA early response genes can be regulated by BR in the same directions. ABA activates BR signal in a fast, limited and short-term manner and the BR-biosynthesis regulatory gene, OsGSR1, plays a key role during this process, whose expression is induced slightly by ABA through transcriptional factor ABI3. Moreover, the early short-term BR signal activation is also important for ABA-mediated salt stress tolerance. Intriguingly, the process and effect of short-term BR signal activation were covered by high concentration of ABA, implying adaptive mechanisms existed in plants to cope with varying degrees of stress.

Mutation of a Nucleotide-Binding Leucine-Rich Repeat Immune Receptor-Type Protein Disrupts Immunity to Bacterial Blight.

Most characterized plant resistance proteins belong to the nucleotide-binding domain and Leu-rich repeat-containing (NLR) family. NLRs are present in an auto-inhibited state in the absence of specific pathogens, while gain-of-function mutations in NLRs usually cause autoimmunity. Here, we show that a gain-of-function mutation, weaker defense (wed), which caused a Phe-to-Leu substitution in the nucleotide-binding domain of a typical NLR in rice (Oryza sativa), led to enhanced susceptibility to Xanthomonas oryzae pv. Oryzae The unexpected accumulation of salicylic acid (SA), along with downregulation of NONEXPRESSOR OF PR1 (NPR1), in wed indicates the potential presence of a feedback regulation loop of SA biosynthesis in rice. Epistasis analyses illustrated that SA accumulation and the NLR-associated components RAR1, OsRac1, and PhyB are dispensable for the wed phenotypes. Intriguingly, besides pattern-triggered immunity, effector-triggered immunity conferred by different resistance proteins, including Xa3/Xa26, Xa4, and Xa21, was also disturbed by wed to a certain extent, indicating the existence of shared regulatory mechanisms for various defense systems. The identification of wed therefore provides a unique system for genetic dissection of shared immune signaling pathways activated by different types of immune receptors.