Pectin Methylesterases: Cell Wall Remodeling Proteins Are Required for Plant Response to Heat Stress

Abstract

Heat stress (HS) is expected to be of increasing worldwide concern in the near future, especially with regard to crop yield and quality as a consequence of rising or varying temperatures as a result of global climate change. HS response (HSR) is a highly conserved mechanism among different organisms but shows remarkable complexity and unique features in plants. The transcriptional regulation of HSR is controlled by HS transcription factors (HSFs) which allow the activation of HS-responsive genes, among which HS proteins (HSPs) are best characterized. Cell wall remodeling constitutes an important component of plant responses to HS to maintain overall function and growth; however, little is known about the connection between cell wall remodeling and HSR. Pectin controls cell wall porosity and has been shown to exhibit structural variation during plant growth and in response to HS. Pectin methylesterases (PMEs) are present in multigene families and encode isoforms with different action patterns by removal of methyl esters to influencing the properties of cell wall. We aimed to elucidate how plant cell walls respond to certain environmental cues through cell wall-modifying proteins in connection with modifications in cell wall machinery. An overview of recent findings shed light on PMEs contribute to a change in cell-wall composition/structure. The fine-scale modulation of apoplastic calcium ions (Ca2+) content could be mediated by PMEs in response to abiotic stress for both the assembly and disassembly of the pectic network. In particular, this modulation is prevalent in guard cell walls for regulating cell wall plasticity as well as stromal aperture size, which comprise critical determinants of plant adaptation to HS. These insights provide a foundation for further research to reveal details of the cell wall machinery and stress-responsive factors to provide targets and strategies to facilitate plant adaptation.

Immunoprofiling of Cell Wall Carbohydrate Modifications During Flooding-Induced Aerenchyma Formation in Fabaceae Roots

“…The presence of DME homogalacturonan in TLCs primary walls has not been previously described and is likely due to action of pectin methylesterase activity upon the homogalacturonan backbone. Removal of methyl esters from homogalacturonan promotes hydrolytic enzyme activity required for "loosening" of primary cell walls prior to wall expansion (Foster, 1967;Micco et al, 2016;Wu et al, 2018) and is a possible prerequisite for expansion of TLCs into the aerenchyma cavity. Additionally, de-methylesterification of pectin may permit enlargement of TLCs prior to development of secondary wall patterning (Goulao et al, 2011), as suggested by cell wall morphology observed in the present study (Supplemental Figure 5)…”

Plant Cell Walls Tackling Climate Change: Biotechnological Strategies to Improve Crop Adaptations and Photosynthesis in Response to Global Warming

“…In contrast, the overexpression of PMEI13 (At5g62360) in Arabidopsis induced tolerance to salinity stress. Transgenic lines presented higher rates of germination and enhanced root growth and overall viability when exposed to salt stress as compared with WT plants [112]. Pectin acetylesterase (PAE) modulate pectin acetylation on their C2 or C3 of galacturonic acid residues.…”

“…Among them, pectins are crucial elements for plant tolerance to high temperatures, as reported in many species such as bromeliad (Nidularium minutum), Arabidopsis, oilseed rape (Brassica napus var. oleifera), and rice [112,[190][191][192]. It has been well reported that the DM of pectins is regulated by the action of PMEs in the cytosol.…”

“…Thus, PMEs positively influence tolerance to elevated temperatures by maintaining proper apoplastic Ca 2+ levels [193]. High temperature activation of PME activity induces the removal of Ca 2+ bridges from homogalacturonan backbound upon heat stress tolerance by activating the expression of certain HSPs to induce CW remodeling in order to maintain plasma membrane integrity [112]. For example, the Arabidopsis PME34 mutant plants, presented thermotolerance impairment.…”

The cell-wall-localised BETA-XYLOSIDASE 4 contributes to immunity of Arabidopsis against Botrytis cinerea

“…The complexity of pectin is generated by a plethora of proteins with most of them being localized in the Golgi (Harholt et al, 2010). However, pectin can also be remodelled in mura (Micheli, 2001; Bosch, 2005) giving the plant more flexibility in the regulation of its cell wall architecture (Rui et al, 2018; Wu et al, 2018). Previous data on the cell wall proteome of Arabidopsis leaves expressing a P. syringae effector AvrRpm1 indicated that BXL4 is such an enzyme acting in mura (Breitenbach et al, 2014).…”