Chloroplast Localized FIBRILLIN11 Is Involved in the Osmotic Stress Response during Arabidopsis Seed Germination

SIMPLE SUMMARY: The FIBRILLIN11 (FBN11) of Arabidopsis has a lipid-binding FBN domain and a kinase domain. FBN11 is present in chloroplasts and is involved in salt and osmotic stress responses during seed germination. In mannitol, the seed germination rate of the fbn11 mutants significantly reduced compared to that of the wild type. The ABA-dependent and -independent stress response regulating genes were differentially expressed in fbn11 mutants and wild-type when grown in mannitol supplemented medium. These results suggest that chloroplast localized FBN11 is involved in mediating osmotic stress tolerance through the signaling pathway that regulates the stress response in the nucleus. ABSTRACT: Plants live in ever-changing environments, facing adverse environmental conditions including pathogen infection, herbivore attack, drought, high temperature, low temperature, nutrient deficiency, toxic metal soil contamination, high salt, and osmotic imbalance that inhibit overall plant growth and development. Plants have evolved mechanisms to cope with these stresses. In this study, we found that the FIBRILLIN11 (FBN11) gene in Arabidopsis, which has a lipid-binding FBN domain and a kinase domain, is involved in the plant’s response to abiotic stressors, including salt and osmotic stresses. FBN11 protein localizes to the chloroplast. FBN11 gene expression significantly changed when plants were exposed to the abiotic stress response mediators such as abscisic acid (ABA), sodium chloride (NaCl), and mannitol. The seed germination rates of fbn11 homozygous mutants in different concentrations of mannitol and NaCl were significantly reduced compared to wild type. ABA-dependent and -independent stress response regulatory genes were differentially expressed in the fbn11 mutant compared with wild type when grown in mannitol medium. These results suggest a clear role for chloroplast-localized FBN11 in mediating osmotic stress tolerance via the stress response regulatory signaling pathway in the nucleus.