Figure 4. Sensing and primary signalling events of heat stress
at the plasma membrane.
In response to heat stress, several plasma membrane-linked protein
activities are triggered which lead to intracellular signals that
collectively regulate the heat stress response in plants. 1. Heat
perception gives rise to increases in Ca2+, which can
enter the cytosol from the apoplast through channels such as CNGC6. This
channel might be activated by cAMP, which is generated by a
transmembrane adenylyl cyclase (tmAC) perhaps activated under heat
stress as membrane fluidity increases. Through association with
calmodulin (CaM), Ca2+ can negatively regulate CNGC6,
and promote the function of HSFs. HSFs are the primary regulators of the
heat response leading to transcriptional induction of HSPs and other
genes. Apart from CNGC6, Annexin 1 (ANN1) is required for cytosolic
increases in Ca2+. 2. The second major factor in the
heat stress response is H2O2, which is
generated by the plasma membrane microdomain NADPH oxidase, RBOHD, whose
activity is modulated by several factors, including
Ca2+ and PA. After
H2O2 enters the cell, it modifies the
PLDδ protein such that it becomes sensitive to activation by
Ca2+. 3. PLDδ generates PA, which has a myriad of
signaling functions which are mediated by its interaction with cytosolic
target proteins. PLDδ is attached to microtubules and its activity leads
to microtubule depolymerization. Moreover,
H2O2 can activate HSFs through MAPK
signaling. 4. PLC3 and PLC9 are required for sHSP induction and
thermotolerance. Most likely, they hydrolyze PIP to generate DAG,
releasing the inositol-bisphosphate (IP2) headgroup. DAG
can be phosphorylated to PA by diacylglycerol kinase (DGK). In plants,
rather than IP2 or IP3, inositol’s more
highly phosphorylated derivatives are the likely inducers of cytosolic
release of Ca2+. DAG could associate with
synaptotagmin (SYT) in the ER at ER-PM contact sites, which may function
to stabilize the plasma membrane under stress, and facilitate the
exchange of lipids between the plasma membrane and the cortical ER. 5.
Besides PA, also PIP2 accumulates under heat stress,
through PIP kinase (PIPK) activity, first only in the plasma membrane,
later also in internal membranes, including the nuclear envelope.
PIP2 regulates effector proteins through specific
lipid-binding domains.