TITLE:
Oxidative Stress Responsive SERK1 Gene Directs the Progression of Somatic Embryogenesis in Cotton (Gossypium hirsutum L. cv. Coker 310)
AUTHORS:
Dhananjay K. Pandey, Bhupendra Chaudhary
KEYWORDS:
Cotton; Somatic Embryogenesis; SERK; Antioxidant
JOURNAL NAME:
American Journal of Plant Sciences,
Vol.5 No.1,
January
13,
2014
ABSTRACT: 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.