Figure 3. Sensing and signaling of heat stress at the
chloroplast.
Exposure to moderate heat has various direct consequences for
chloroplast proteins and membranes, which trigger rescue pathways. In
the thylakoidal membrane, LHCII proteins aggregate, which leads to an
excess of its major constituent, the non-bilayer prone glycerolipid
MGDG. As a consequence, a non-bilayer structure (the HII phase) emerges,
which consists of MGDG organized in hexagonal, stacked tubules. The
xanthophyll cycle enzyme, violaxanthin de-epoxidase (VDE), recruits
specifically to the HII phase in the thylakoid lumen, catalyzing the
synthesis of zeaxanthin (ZEA) from its precursors, violaxanthin (VIO)
and antheraxanthin (ANT). The HII phase remains attached, which allows
for free diffusion of the photoprotective xanthophylls to the thylakoid.
VIPP1 and sHSP recruit to the thylakoid membrane under heat stress, as
they recognize membrane packing defects. They protect thylakoid membrane
and PSII integrity. Heat stress is signalled in the chloroplast by a
rapid Ca2+ increase in the stroma which depends on the
activity of the calcium sensor CAS. Furthermore, heat induces breakdown
of the envelope desaturase FAD8, responsible for synthesis of
polyunsaturated fatty acids. This causes an adaptive decrease in
membrane desaturation. The isoprenoid biosynthesis intermediate MEcPP
accumulates due to a heat-induced bottleneck in the pathway. MEcPP,
together with H2O2 resulting from excess
excitation energy, and other stress-induced molecules, serve as
retrograde signals to regulate heat stress genes in the nucleus.