Abstract
Pectin is a major component of the plant cell wall, forming a network that contributes to cell wall integrity and flexibility. Pectin methylesterase (PME) catalyzes the removal of methylester groups from the homogalacturonan backbone, the most abundant pectic polymer, and contributes to intercellular adhesion during plant development and different environmental stimuli stress. In this study, we identified and characterized an Arabidopsis type-II PME, PME53, which encodes a cell wall deposited protein and may be involved in the stomatal lineage pathway and stomatal functions. We demonstrated that PME53 is expressed explicitly in guard cells as an abscisic acid (ABA)-regulated gene required for stomatal movement and thermotolerance. The expression of PME53 is significantly affected by the stomatal differentiation factors SCRM and MUTE. The null mutation in PME53 results in a significant increase in stomatal number and susceptibility to ABA-induced stomatal closure. During heat stress, the pme53 mutant highly altered the activity of PME and significantly lowered the expression level of the calmodulin AtCaM3, indicating that PME53 may be involved in Ca2+-pectate reconstitution to render plant thermotolerance. Here, we present evidence that the PME53-mediated de-methylesterification status of pectin is directed toward stomatal development, movement, and regulation of the flexibility of the guard cell wall required for the heat response.
Highlights
Plants are sessile organisms that have to cope with the challenge of extreme environmental conditions, including various abiotic and biotic stresses, all of which exert adverse effects on plant growth and development
We showed that the expression of PME53 increased significantly after treatment with 100 μM abscisic acid (ABA) for 1 h in guard cells, but not in mesophyll cells (Supplementary Figure 1)
Seven-day-old Arabidopsis seedlings subjected to ABA, salt, and osmotic treatments were conducted, and PME53 expression levels were analyzed by Quantitative real-time PCR (q-PCR) (Figure 1A and Supplementary Figure 2)
Summary
Plants are sessile organisms that have to cope with the challenge of extreme environmental conditions, including various abiotic and biotic stresses, all of which exert adverse effects on plant growth and development. The most likely negative impact of these changes is an increase in temperature, which directly impacts DNA, proteins, cell membranes, and metabolism processes, severely limiting plant growth, development, and productivity. The induction of molecular chaperone heat shock proteins (HSPs) is an essential part of the universally conserved heat response, allowing organisms to survive stress conditions such as elevated temperatures that cause protein unfolding (Lindquist and Craig, 1988). Apart from the well-known heat stress response, little is known about how the dynamics of plant cell wall changes in wall composition and architecture are associated with various stresses. The plant cell wall is a sophisticated structure formed by a complex mixture of polysaccharide-rich proteins and other polymers assembled into a rigid, flexible, and dynamically organized network (Wolf et al, 2009; Wu et al, 2018). The maintenance of cell wall integrity is essential for cell viability and function during stress (Hamann et al, 2009; Wu et al, 2018)
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