Genome-Wide Analysis of MDHAR Gene Family in Four Cotton Species Provides Insights into Fiber Development via Regulating AsA Redox Homeostasis

Abstract

Monodehydroasorbate reductase (MDHAR) (EC1.6.5.4), a key enzyme in ascorbate-glutathione recycling, plays important roles in cell growth, plant development and physiological response to environmental stress via control of ascorbic acid (AsA)-mediated reduction/oxidation (redox) regulation. Until now, information regarding <i>MDHAR</i> function and regulatory mechanism in <i>Gossypium</i> have been limited. Herein, a genome-wide identification and comprehensive bioinformatic analysis of 36 <i>MDHAR</i> family genes in four <i>Gossypium</i> species, <i>Gossypium arboreum</i>, <i>G. raimondii, G. hirsutum</i>, and <i>G. barbadense</i>, were performed, indicating their close evolutionary relationship. Expression analysis of <i>GhMDHARs</i> in different cotton tissues and under abiotic stress and phytohormone treatment revealed diverse expression features. Fiber-specific expression analysis showed that <i>GhMDHAR1A/D</i>, <i>3A/D</i> and <i>4A/D</i> were preferentially expressed in fiber fast elongating stages to reach peak values in 15-DPA fibers, with corresponding coincident observances of MDHAR enzyme activity, AsA content and ascorbic acid/dehydroascorbic acid (AsA/DHA) ratio. Meanwhile, there was a close positive correlation between the increase of AsA content and AsA/DHA ratio catalyzed by MDHAR and fiber elongation development in different fiber-length cotton cultivars, suggesting the potential important function of MDHAR for fiber growth. Following H₂O₂ stimulation, <i>GhMDHAR</i> demonstrated immediate responses at the levels of mRNA, enzyme, the product of AsA and corresponding AsA/DHA value, and antioxidative activity. These results for the first time provide a comprehensive systemic analysis of the <i>MDHAR</i> gene family in plants and the four cotton species and demonstrate the contribution of MDHAR to fiber elongation development by controlling AsA-recycling-mediated cellular redox homeostasis.