Excessive cadmium (Cd) accumulation in grains of rice (Oryza sativa L.) is a risk to food security. The transporters in the nodes of rice are involved in the distribution of mineral elements including toxic elements to different tissues such as grains. However, the mechanism of Cd accumulation in grains is largely unknown. Here, we report a node-expressed transporter gene, OsCCX2, a putative cation/calcium (Ca) exchanger, mediating Cd accumulation in the grains of rice. Knockout of OsCCX2 caused a remarkable reduction of Cd content in the grains. Further study showed that disruption of this gene led to a reduced root-to-shoot translocation ratio of Cd. Moreover, Cd distribution was also disturbed in different levels of internode and leaf. OsCCX2 is localized to plasma membrane, and OsCCX2 is mainly expressed in xylem region of vascular tissues at the nodes. OsCCX2 might function as an efflux transporter, responsible for Cd loading into xylem vessels. Therefore, our finding revealed a novel Cd transporter involved in grain Cd accumulation, possibly via a Ca transport pathway in the nodes of rice.

Summary: Leaf morphogenesis is a crucial process in plants that governs essential physiological functions such as photosynthesis and transpiration. Despite significant advances in understanding leaf development, the mechanism of intricate cellular patterning remains elusive. We characterize the OsLC1 mutant, which displays a curly leaf phenotype alongside reductions in plant height and tiller number, which are indicative of multiple morphological abnormalities. Through map‐based cloning, we identified OsLC1 as encoding a transaldolase (TA) protein, whose genetic variations in OsLC1 lead to the disruptions of cell patterning across the vasculature, bundle sheath cells, mesophyll, stomata, bulliform cells and sclerenchyma cells. OsLC1 exhibited TA activity and modulated metabolic flux to the shikimic pathway, thereby affecting phenylpropanoid metabolism. This regulation influenced lignin and flavonoid biosynthesis, ultimately modulating cellular pattern formation through perturbations to flavonoid‐mediated auxin or lignin homeostasis. Notably, loss of OsLC1 function led to a reduction in leaf water status, which, along with abnormal cellular patterns in oslc1, caused leaf curling. Overall, our findings provide insights into the regulatory mechanisms underlying cell patterning in the leaf and offer valuable perspectives on leaf morphogenesis in rice.

During double fertilization of angiosperms, the central cell of the female gametophyte fuses with a sperm cell to produce the endosperm, a storage tissue that nourishes the developing embryo within the seed. Although many genetic mutants defective in female gametophytic functions have been characterized, the molecular mechanisms controlling the specification and differentiation of the central cell are still not fully understood. Here, we report a mitochondrial ribosomal protein, RPS9M, is required for central cell maturation. RPS9M was highly expressed in the male and female gametophytes before and after double fertilization. The female gametophytes were defective in the rps9m mutant specifically concerning maturation of central cells. The morphological defects include unfused polar nuclei and smaller central vacuole in central cells. In addition, embryo initiation and early endosperm development were also severely affected in rps9m female gametophytes even after fertilized with wild type pollens. The RPS9M can interact with ANK6, an ankyrin-repeat protein in mitochondria previously reported to be required for fertilization. The expression pattern and mutant phenotype of RPS9M are similar to those of ANK6 as well, suggesting that RPS9M may work together with ANK6 in controlling female gametophyte development, possibly by regulating the expression of some mitochondrial proteins.