TY - JOUR
T1 - Heat shock response in photosynthetic organisms
T2 - Membrane and lipid connections
AU - Horváth, Ibolya
AU - Glatz, Attila
AU - Nakamoto, Hitoshi
AU - Mishkind, Michael L.
AU - Munnik, Teun
AU - Saidi, Yonousse
AU - Goloubinoff, Pierre
AU - Harwood, John L.
AU - Vigh, László
N1 - Funding Information:
This work was supported in part by Grant-in-aids for Scientific Research (C) (No. 16570028 ) to H.N. from the Ministry of Education, Science, Sports and Culture of Japan, by Hungarian Basic Research Fund to I.H. A.G. and L.V. (OTKA, No. K84257 and No. 82097), by MTA-JSPS (No. 122) and by the Hungarian National Development Agency TAMOP-4.2.2/08/1-2008-0014.
PY - 2012/7
Y1 - 2012/7
N2 - The ability of photosynthetic organisms to adapt to increases in environmental temperatures is becoming more important with climate change. Heat stress is known to induce heat-shock proteins (HSPs) many of which act as chaperones. Traditionally, it has been thought that protein denaturation acts as a trigger for HSP induction. However, increasing evidence has shown that many stress events cause HSP induction without commensurate protein denaturation. This has led to the membrane sensor hypothesis where the membrane's physical and structural properties play an initiating role in the heat shock response. In this review, we discuss heat-induced modulation of the membrane's physical state and changes to these properties which can be brought about by interaction with HSPs. Heat stress also leads to changes in lipid-based signaling cascades and alterations in calcium transport and availability. Such observations emphasize the importance of membranes and their lipids in the heat shock response and provide a new perspective for guiding further studies into the mechanisms that mediate cellular and organismal responses to heat stress.
AB - The ability of photosynthetic organisms to adapt to increases in environmental temperatures is becoming more important with climate change. Heat stress is known to induce heat-shock proteins (HSPs) many of which act as chaperones. Traditionally, it has been thought that protein denaturation acts as a trigger for HSP induction. However, increasing evidence has shown that many stress events cause HSP induction without commensurate protein denaturation. This has led to the membrane sensor hypothesis where the membrane's physical and structural properties play an initiating role in the heat shock response. In this review, we discuss heat-induced modulation of the membrane's physical state and changes to these properties which can be brought about by interaction with HSPs. Heat stress also leads to changes in lipid-based signaling cascades and alterations in calcium transport and availability. Such observations emphasize the importance of membranes and their lipids in the heat shock response and provide a new perspective for guiding further studies into the mechanisms that mediate cellular and organismal responses to heat stress.
KW - Heat shock response
KW - Membrane fluidizer
KW - Membrane sensor hypothesis
KW - Molecular chaperones
KW - Phosphatidic acid
KW - Phosphatidylinositol 4,5-bisphosphate
KW - Signaling lipids
KW - Small heat shock proteins
KW - Transient Ca influx
UR - http://www.scopus.com/inward/record.url?scp=84859932485&partnerID=8YFLogxK
U2 - 10.1016/j.plipres.2012.02.002
DO - 10.1016/j.plipres.2012.02.002
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C2 - 22484828
AN - SCOPUS:84859932485
SN - 0163-7827
VL - 51
SP - 208
EP - 220
JO - Progress in Lipid Research
JF - Progress in Lipid Research
IS - 3
ER -