Membrane lipid composition affects plant heat sensing and modulates Ca²⁺-dependent heat shock response

Abstract

In the context of the current global warming, an increase in the global temperature and in the frequency and severity of heat waves is expected to affect crops productivity and distribution. [1][2][3][4] Land plants constantly encounter wide daily and seasonal thermal variations and the agricultural yields are tightly correlated to their effective tolerance to thermal stress. 5,6 To face this environmental challenge and develop new strategies, it is crucial to fully understand the mechanisms by which mild variations in ambient temperature are accurately perceived, leading to a timely activation of the heat shock proteins (HSPs) and the establishment of an optimal thermotolerance. Temperature sensing in plants and other organisms has been the subject of numerous studies. 5-7 For many years, the activation of HSPs following a sharp temperature increase was thought to be regulated by denatured cytosolic proteins, that upon sequestering Hsp70 and Hsp90, would derepress heat shock transcription factors (HSFs), thereby inducing the upregulation of heat shock genes. [8][9][10] Yet, the overexpression of HSPs, so called the heat shock response (HSR), can be activated under mild physiological conditions that are unlikely to cause any protein denaturation in the cell. [11][12][13] Although multiple HSR triggering mechanisms may co-exist, 6,14-16 recent evidences in bacteria, algae, plants and mammalian cells point at the understanding how plants sense and respond to heat stress is central to improve crop tolerance and productivity. recent findings in Physcomitrella patens demonstrated that the controlled passage of calcium ions across the plasma membrane regulates the heat shock response (hSr). to investigate the effect of membrane lipid composition on the plant hSr, we acclimated P. patens to a slightly elevated yet physiological growth temperature and analysed the signature of calcium influx under a mild heat shock. Compared to tissues grown at 22°C, tissues grown at 32°C had significantly higher overall membrane lipid saturation level and, when submitted to a short heat shock at 35°C, displayed a noticeably reduced calcium influx and a consequent reduced heat shock gene expression. these results show that temperature differences, rather than the absolute temperature, determine the extent of the plant hSr and indicate that membrane lipid composition regulates the calcium-dependent heat-signaling pathway.

The Effect of Supplemental Irrigation on Canopy Temperature Depression, Chlorophyll Content, and Water Use Efficiency in Three Wheat (Triticum aestivum L. and T. durum Desf.) Varieties Grown in Dry Regions of Jordan

“…Furthermore, the reduction in grain yield under the rain-fed treatment in the current study could be attributed to the findings of Saidi et al [70], who showed that a significant reduction in grain yield in rain-fed conditions may result from reducing the production of photo-assimilates for grain filling, reducing the sink power in absorbing photo-assimilates and reducing the grain filling duration. Obviously, water stress hastens maturation and decreases photosynthesis, leading to lower grain yield.…”

Plasma Membrane Cyclic Nucleotide Gated Calcium Channels Control Land Plant Thermal Sensing and Acquired Thermotolerance

“…It is therefore essential that plant cells can sense small increments of ambient temperatures and integrate these changes into an effective HSR. This proceeds in the form of the timely accumulation of protective metabolites and heat shock proteins , many of which are molecular chaperones that efficiently protect thermolabile macromolecules, in particular components of the photosynthetic apparatus (Heckathorn et al, 1998;Salvucci, 2008), and rehabilitate cell proteostasis in general (Finka et al, 2010). …”

“…Highly sensitive molecular thermosensors involving both a protein and a plasma membrane component have been identified in the plasma membrane of the moss Physcomitrella patens (Saidi et al, 2009(Saidi et al, , 2010. Heat causes a transient opening of Ca 2+ channels, allowing a specific inward flux of extracellular Ca 2+ ions from the apoplast (Wu et al, 2010) possibly via modulation of membrane fluidity (Saidi et al, 2009).…”

Patterns of thermotolerance, chlorophyll fluorescence, and heat shock gene expression vary among fourBoecheraspecies andArabidopsis thaliana

“…Many of the HSPs are chaperone proteins and assist in the proper folding or refolding of target proteins (Craig et al 1994;Boston et al 1996;Hartl et al 2011;Kim et al 2013). The presence of HSPs within cells is correlated with organismal thermotolerance (von Kotak et al 2007;Larkindale and Vierling 2008;Saidi et al 2010).…”