Oxidative Stress Responsive <i>SERK1</i>Gene Directs the Progression of Somatic Embryogenesis in Cotton (<i>Gossypium hirsutum</i>L. cv. Coker 310)

• 作者: Bhupendra Chaudhary Dhananjay K. Pandey
• 来源期刊: 美国植物学期刊(英文)
• 学科: 医学
• 关键词: COTTON Somatic Embryogenesis SERK Antioxidant
• 年，卷（期）: 2014,（1）
• 页码范围: 80-102
• 页数: 23页
• 分类号: R73

摘要

Somatic embryogenesis (SE) is a prominent mode of regeneration in plants. The acquisition of SE is predominantly invoked by the oxidative stress which plays an important role in signal transduction and cellular redox. Since balanced generation of oxidants is important to cellular differentiation, modulation in cell redox could be responsive to genotypic refinement for SE. To study the dynamics of cellular redox during SE, we conducted comparative expression analyses of cotton (Gossypium hirsutum), using two independently purified near-isogenic lines for the trait of SE. We interrogated expression changes in cell-signaling factor Somatic Embryogenesis Receptor Kinase (SERK) and activity of antioxidant Glutathione in different developmental stages including cotyledonary leaf, calli from different stages of regeneration of fully-regenerating (FR) and non-regenerating (NR) lines of Coker310 cultivar. At evolutionary scale, the cotton SERKs showed high sequence similarity in receptor kinase domain with diverse systems. Exclusively, SERK1 responsible for potential signaling processes during SE revealed significant expression up-regulation in the embryogenic calli of FR line. Similarly, activity of antioxidant glutathione was substantially up-regulated in embryogenic calli of FR line in comparison to its counterpart form. In contrast, calli from early-stages of regeneration of both FR and NR lines had no significant influences on the regulation of SERK and glutathione levels prior to the acquisition of embryogenesis. These results highlight that in vitro purification of FR line in cotton for enhanced regeneration potential (through SE) resulted in signaling and metabolic transformations of the manner in which cellular redox levels have become modulated.