Inhibition of ClCaM2 expression promoted root development in Cunninghamia lanceolata seedlings experiencing...

Phosphorus is a key nutrient limiting terrestrial ecosystem productivity, with low phosphorus availability affecting over 30% of agricultural and forest ecosystems worldwide. Root development plays a central role in enhancing phosphorus uptake efficiency in plants, with root number being a major determinant of adaptation to phosphorus-deficient. Chinese fir (Cunninghamia lanceolata) cuttings originating from the same clone were used in this study. Root phenotyping, exogenous inhibitor treatments, and transcriptome sequencing were conducted to elucidate the mechanisms underlying root responses to phosphorus limitation. Under phosphorus-deficient conditions, seedling root number was 24.8% and 32.7% higher than in the phosphorus-sufficient at a lower level, and phosphorus-sufficient at a higher level, respectively. The calmodulin protein ClCaM2 was also markedly downregulated under phosphorus-deficient conditions. Inhibition of ClCaM2 expression by an exogenous inhibitor increased root number by 26.4% and significantly enhanced root length and surface area by 26.1% and 31.8%, respectively. Treatment with the exogenous inhibitor also led to the upregulation of phosphate transporter genes (1.5-fold) and key auxin signaling genes, suggesting strong growth-promoting effects. In contrast to wild-type seedlings, transgenic white poplar seedlings overexpressing ClCaM2 exhibited reductions in root length, number, surface area, and volume. Thus, ClCaM2 was shown to participate in adaptive Chinese fir root responses to phosphorus deficiency by negatively regulating root development and moderating the expression of phosphate transporter genes. These findings extend our understanding of the molecular regulation of tree root responses to nutrient stress and provide a potential strategy for improving plant tolerance to low-phosphorus stress through the targeted regulation of calcium signaling.