Classically, lichen phycobionts are described as poikilohydric
organisms able to undergo desiccation due to the constitutive
presence of molecular protection mechanisms.
However, little is known about the induction of cellular responses
in lichen phycobionts during drying. The analysis of
the lipid composition of the desiccated lichen microalga
Asterochloris erici revealed the unusual accumulation of
highly polar lipids (oligogalactolipids and phosphatidylinositol),
which prevents the fusion of membranes during stress,
but also the active degradation of cone-shaped lipids (monogalactosyldiacylglycerol
and phosphatidylethanolamine) to
stabilize membranes in desiccated cells. The level of phosphatidic
acid increased 7-fold during desiccation, implicating
a possible role for phospholipase D (PLD) in the response
to osmotic stress. Inhibition of PLD with 1-butanol markedly
impaired the recovery of photosynthesis activity in A. erici
upon desiccation and salt stress (2M NaCl). These two
hyperosmotic stresses caused the phosphorylation of c-Jun
N-terminal kinase (JNK) and p38-like mitogen-activated
protein kinase (MAPK) and the dephosphorylation of extracellular
signal-regulated kinase (ERK). The incubation with
1-butanol reduced the phosphorylation of JNK-like proteins
and increased the dephosphorylation of ERK-like proteins,
which indicates an upstream control of MAPK cascades by
PLD. The phosphoproteome showed that desiccation caused
the phosphorylation of several proteins in A. erici, most of
them involved in protein turnover. The results demonstrate
that lichen phycobionts possess both constitutive and inducible
protective mechanisms to acquire desiccation tolerance.
Among others, these responses are controlled by the
PLD pathway through the activation of MAPK cascades.
