Increasing rice yield has always been one of the primary objectives of rice breeding. However, panicle degeneration, a complex phenomenon regulated by many genetic and environmental factors, often occurs in rice-growing regions and severely curbs rice yield. In this study, we obtained a new apical panicle degeneration mutant named ym48, which induces a marked degeneration rate and diminishes the final grain yield. Cellular and physiological analyses revealed that the apical panicle in ym48 undergoes programmed cell death, accompanied by excessive accumulations of peroxides. Following, the panicle degeneration gene OsCAX1a was identified, which was involved in Ca2+ transport in the ym48 mutant. In OsCAX1a, a relative conserved T to A substitution was noted at the 64th amino acid, which disrupted Ca2+ transport. Hydroponics assays and Ca2+ quantification confirmed that Ca2+ transport and distribution to apical tissues were restricted and over-accumulated in mutant sheath. Ca2+ transport between cytoplasm and vacuole was affected, and the reduced content of Ca2+ in vacuole and cell wall and the decreased of Ca2+ absorption were appeared in ym48 mutant. RNA-Seq data indicated that the abnormal CBL (calcineurin b-like proteins) pathway mediated by deficient Ca2+ might occur in mutant, resulting in the burst of ROS and programmed cell death in panicles. Our results explained the key role of OsCAX1a in Ca2+ transport and distribution and laid a foundation to further explore the genetic and molecular mechanisms of panicle degeneration and the efficiency of Ca2+ fertilization in rice.

Increasing the yield of rice has always been one of the primary purposes of rice breeding. However, panicle degeneration, a complex characteristic regulated by many genes and commonly encountered in rice production, seriously reduces yield. In this study, we obtained a new apical panicle degeneration mutant named ym48, which induces a marked degeneration rate and reduces grain yield in rice. Cellular and physiological analyses revealed that the apical panicle in ym48 undergoes programmed cell death, accompanied by the accumulation of higher levels of peroxide. Next, the OsCAX1a gene, which is responsible for Ca 2+ transportation, was identified, and a highly conserved A to G substitution was noted at the 190 th nucleotide in ym48, which seriously damaged Ca 2+ transport. Through hydroponics assays and Ca 2+ quantification, we found that Ca 2+ transportation and distribution from the underground part to apical tissues was blocked and overaccumulated in mutant stems. In general, this Ca 2+ deficiency mediated by OsCAX1a induced peroxide accumulation and resulted in programmed cell death in the apical panicle of the ym48 mutant. Our results demonstrate the essential role of OsCAX1a in Ca 2+ transportation and distribution, laying a foundation to further explore the genetic and molecular mechanisms of panicle development and differentiation in rice.