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L. Carratu et al.
all vertebrates activates transcription of heat shock genes after temperature
shock, and HSF2 that induces heat shock response during cellular
differentiation, spermatogenesis and embryonic development [31]. In
chicken it has been shown that low levels of HSF2 mRNA in liver and
blood cells correlate with a very low or absent induction of the hsp70
mRNA after heat shock [32]. Therefore, it is reasonable at this stage of
investigation to postulate that different levels of HSFs could be present in
different tissues of Antarctic fish and also in different fish species, which
could explain the lack of expression of hsp70 in T. bernacchii.
Recent evidence suggests that the temperature at which expression of
heat shock genes occurs is influenced by the membrane fluid state which
in tum is regulated by the activity of the f19-desaturase gene [3]. For this
reason it will be crucial to study in detail f19 -desaturase gene regulation and
determine fatty acid content of membranes from different fish tissue to
correlate it to the capacity to induce gene expression.
Our experiments on the differential expression of hsp70 gene confirm
the notion that stenothermal Antarctic species have conserved a low
thermal resistance and suggest that the constant low temperature has
modified the regulation of expression of these highly conserved genes.
This represents, to our knowledge, the first example of a high eukaryotic
organism that has lost the heat shock gene induction in response to the
evolutionary adaptation to the Antarctic Ocean.
Acknowledgments
This work was supported by a Grant from the Italian Antarctic Programme
(PNRA) and by a Grant from CNR Progetto Strategico Stress Cellulare.
References
1. Lindquist S, Craig EA (1988) The heat shock proteins. Ann Rev Genet 22:
631-677
2. Cossins AR, Bowler K (1987) Temperature biology of animals. Chapman &
Hall, New York
3. Carratli L, Franceschelli S, Pardini CL, Kobayashi GS, Horvath I, Vigh L,
Maresca B (1996) Membrane lipid perturbation modifies the set point of the
temperature of heat shock response in yeast. Proc Nat! Acad Sci USA 93:
2120-2125
4. Vigh L, Los DA, Horwath I, Murata N (1993) The primary signal in the
biological perception of temperature: Pd-catalyzed hydrogenation of
membrane lipids stimulated the expression of the desA gene in Synechocystis
PCC6803. Proc Nat! Acad Sci USA 90: 9090-9094
5. Hegner D (1980) Age-dependence of molecular and functional changes in
biological membrane properties. Mech Ageing Dev 12: 207-214
L. Carratu et al.
all vertebrates activates transcription of heat shock genes after temperature
shock, and HSF2 that induces heat shock response during cellular
differentiation, spermatogenesis and embryonic development [31]. In
chicken it has been shown that low levels of HSF2 mRNA in liver and
blood cells correlate with a very low or absent induction of the hsp70
mRNA after heat shock [32]. Therefore, it is reasonable at this stage of
investigation to postulate that different levels of HSFs could be present in
different tissues of Antarctic fish and also in different fish species, which
could explain the lack of expression of hsp70 in T. bernacchii.
Recent evidence suggests that the temperature at which expression of
heat shock genes occurs is influenced by the membrane fluid state which
in tum is regulated by the activity of the f19-desaturase gene [3]. For this
reason it will be crucial to study in detail f19 -desaturase gene regulation and
determine fatty acid content of membranes from different fish tissue to
correlate it to the capacity to induce gene expression.
Our experiments on the differential expression of hsp70 gene confirm
the notion that stenothermal Antarctic species have conserved a low
thermal resistance and suggest that the constant low temperature has
modified the regulation of expression of these highly conserved genes.
This represents, to our knowledge, the first example of a high eukaryotic
organism that has lost the heat shock gene induction in response to the
evolutionary adaptation to the Antarctic Ocean.
Acknowledgments
This work was supported by a Grant from the Italian Antarctic Programme
(PNRA) and by a Grant from CNR Progetto Strategico Stress Cellulare.
References
1. Lindquist S, Craig EA (1988) The heat shock proteins. Ann Rev Genet 22:
631-677
2. Cossins AR, Bowler K (1987) Temperature biology of animals. Chapman &
Hall, New York
3. Carratli L, Franceschelli S, Pardini CL, Kobayashi GS, Horvath I, Vigh L,
Maresca B (1996) Membrane lipid perturbation modifies the set point of the
temperature of heat shock response in yeast. Proc Nat! Acad Sci USA 93:
2120-2125
4. Vigh L, Los DA, Horwath I, Murata N (1993) The primary signal in the
biological perception of temperature: Pd-catalyzed hydrogenation of
membrane lipids stimulated the expression of the desA gene in Synechocystis
PCC6803. Proc Nat! Acad Sci USA 90: 9090-9094
5. Hegner D (1980) Age-dependence of molecular and functional changes in
biological membrane properties. Mech Ageing Dev 12: 207-214