Role of callose accumulation in the suppression of calcium-deficiency-induced necrosis in <i>Arabidopsis thaliana</i> cotyledons

Calcium (Ca) deficiency symptoms, such as blossom end rot in tomato and tip burn in lettuce, are among the most serious physiological disorders in agriculture. A common feature of this disorder is the expansion of necrosis. However, mechanisms underlying Ca-deficiency-induced necrosis remain poorly understood. We previously identified callose synthase genes (<i>GSL1</i>, <i>GSL8</i>, <i>GSL10</i>) as the causal genes of low-Ca-sensitive <i>Arabidopsis thaliana</i> mutants, which exhibit severe cell death in true leaves and reduced callose accumulation in cotyledons under low-Ca conditions. This raises the question of whether callose accumulation suppresses the spread of cell death. To clarify their relationship within the same organ, we examined callose deposition and cell death in the cotyledons of the <i>gsl10</i> mutant. Although the <i>gsl10</i> mutant showed a comparable level of total cell death to wild-type plants, the necrotic spots were larger. Furthermore, the largest necrotic spots were typically found at the cotyledon tip, but this tendency was weaker in <i>gsl10</i> mutant. Collectively, our results suggest that callose does not suppress the initiation of cell death but rather limits its propagation, thereby leading to the formation of a characteristic necrotic pattern preferentially occurring at the cotyledon tip.