These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Overexpression of the Stress-Inducible SsMAX2 Promotes Drought and Salt Resistance via the Regulation of Redox Homeostasis in Arabidopsis.
    Author: Wang Q, Ni J, Shah F, Liu W, Wang D, Yao Y, Hu H, Huang S, Hou J, Fu S, Wu L.
    Journal: Int J Mol Sci; 2019 Feb 15; 20(4):. PubMed ID: 30781340.
    Abstract:
    Recent studies have demonstrated that strigolactones (SLs) also participate in the regulation of stress adaptation; however, the regulatory mechanism remains elusive. In this study, the homolog of More Axillary Branches 2, which encodes a key component in SL signaling, in the perennial oil plant Sapium sebiferum was identified and functionally characterized in Arabidopsis. The results showed that the expression of SsMAX2 in S. sebiferum seedlings was stress-responsive, and SsMAX2 overexpression (OE) in Arabidopsis significantly promoted resistance to drought, osmotic, and salt stresses. Moreover, SsMAX2 OE lines exhibited decreased chlorophyll degradation, increased soluble sugar and proline accumulation, and lower water loss ratio in response to the stresses. Importantly, anthocyanin biosynthesis and the activities of several antioxidant enzymes, such as superoxide dismutase (SOD), peroxidase (POD), and ascorbate peroxidase (APX), were enhanced in the SsMAX2 OE lines, which further led to a significant reduction in hydrogen peroxide levels. Additionally, the SsMAX2 OE lines exhibited higher expression level of several abscisic acid (ABA) biosynthesis genes, suggesting potential interactions between SL and ABA in the regulation of stress adaptation. Overall, we provide physiological and biochemical evidence demonstrating the pivotal role of SsMAX2 in the regulation of osmotic, drought, and salt stress resistance and show that MAX2 can be a genetic target to improve stress tolerance.
    [Abstract] [Full Text] [Related] [New Search]