ABSTRACT Zinc (Zn) homeostasis is essential for plant growth; yet, how zinc‐deficiency‐triggered calcium (Ca) signals are decoded into homeostatic adjustments remains elusive. Here, we identify the calcium‐dependent protein kinase 10 (CPK10) as a key decoder of zinc‐deficiency‐triggered Ca 2+ signals. Under zinc‐deficient conditions, both the protein level and the kinase activity of CPK10 increase. Subsequently, CPK10 interacts with and phosphorylates the zinc‐sensing transcription factors bZIP19 and bZIP23, thereby repressing their DNA‐binding and transcriptional activities. Zrt/Irt‐like protein (ZIP) family members are the primary transporters responsible for zinc uptake from the soil, and CPK10‐mediated phosphorylation of bZIP19 and bZIP23 reduces the expression of ZIP1 , ZIP4 , and defensin‐like (DEFL) genes such as DEFL208 . CPK10 activation is time‐delayed, peaking at 72 h after zinc‐deficiency treatment, providing a braking mechanism that prevents prolonged high‐rate ion flux driven by sustained high‐level expression of zinc transporters. The CPK10‐targeted phosphorylation site Ser241 of bZIP19 is conserved in dicots but absent in monocots, suggesting evolutionary divergence in this zinc homeostasis‐regulatory module. Our work reveals a Ca 2+ –CPK10–bZIP19/23 module that mediates spatiotemporal control of zinc homeostasis, highlighting a key regulatory layer in plant nutrient signaling.
Editing TaBADH1 alone or TaBADH1 and TaBADH2 via CRISPR/Cas9 produced fragrant wheat with up to 11.24-fold higher 2-acetyl-1-pyrroline than the wild type without yield penalty, revealing asymmetric functional redundancy between these two genes and providing elite germplasm for wheat quality improvement.
ABSTRACT Soybean ( Glycine max [L.] Merr.) was domesticated in China over five millennia ago; yet, its global expansion has resulted in two distinct, independently evolved breeding pools in China and the Americas. While regional breeding has optimized specific traits, a comprehensive roadmap for the reciprocal exchange of these “breeding‐specific” beneficial alleles is lacking. Here, we performed a large‐scale genomic dissection of 2,377 soybean accessions, integrating 8.4 million high‐quality SNPs with multi‐environment phenotyping across 11 locations. Through genome‐wide association studies (GWAS), we identified 261 significant loci (223 novel) governing six key agronomic traits, revealing that Chinese and American germplasms have accumulated distinct sets of beneficial alleles of seed size/protein in China and oil/yield in the Americas. To harness this untapped potential, we developed the Soybean Targeted Improvement Navigation System (STINS), a framework integrating population genomics, GWAS, and genomic selection (GS). We demonstrate the potential of targeted beneficial allele introgression between populations via gene modification for rapid trait improvement. Proof‐of‐concept functional evaluation through CRISPR/Cas9‐mediated knockout of GmST05 in an American cultivar and overexpression of a resistant GmSNAP18 haplotype in a Chinese cultivar provided experimental support for STINS‐predicted targets for protein content and SCN resistance improvement. Our study provides a navigable genomic resource for “knowledge‐driven design breeding”, offering a blueprint for the global exchange of elite alleles to ensure future food security.
ABSTRACT Apple Alternaria blotch, caused by Alternaria alternata f. sp. mali ( A. alternata ), is a devastating fungal disease threatening global apple production. However, the early signaling pathway underlying apple resistance to A. alternata remains unclear. In this study, through transcriptomic analysis, we identified that MdWRKY9 is a key positive regulator of apple resistance to A. alternata , whose expression is induced in the resistant “Hanfu” while being reduced in the susceptible “Gala” following A. alternata infection. Stable overexpression of MdWRKY9 enhanced apple resistance to A. alternata , whereas RNA interference (RNAi)‐mediated knockdown of MdWRKY9 increased susceptibility. We further demonstrated that MdWRKY9 directly represses the expression of MdJAZ8 , a key repressor of jasmonate (JA) signaling. Accordingly, stable overexpression of MdJAZ8 in apple calli reduced resistance to A. alternata and suppressed JA signaling. Consistently, transient overexpression of MdJAZ8 in apple leaves decreased resistance to A. alternata , whereas transient silencing of MdJAZ8 via RNAi enhanced disease resistance. Furthermore, we identified that the receptor‐like cytoplasmic kinase MdBIK1 ( BOTRYTIS ‐INDUCED KINASE1, a core component of the PTI pathway) interacts with and phosphorylates MdWRKY9 at Thr‐2. The phosphorylation of MdWRKY9 enhances resistance to A. alternata by further suppressing MdJAZ8 and activating JA signaling. Together, our findings define a complete PTI‐associated signaling module in which the MdBIK1–MdWRKY9 complex enhances JA‐mediated immunity against A. alternata by directly repressing MdJAZ8 . This study refines the regulatory mechanism by which the BIK1 family kinases modulate JA signaling, providing new insights into the plant immune signaling network.
