STRESS RESPONSES - Cyanobacteria - page 673

of isiB which was co-transcribed with isiB . The involvement of isiB and isiC in countering oxidative
stress and the role of isiA and isiB in the management of heat and light stresses immediately after
heat shock have been stressed. The optimization of light energy supply after a heat shock seems
to be an essential step in preventing cellular damage as well as in the recovery from heat stress
(Kojima et al ., 2006).
v) Regulation of Hsp synthesis : Heat shock responses involve protein unfolding and malfunction
leading to cell death. The synthesis of Hsps counters this effect by refolding the denatured proteins
and the proteases degrade those proteins which are not recoverable. The regulation of Hsp synthesis
is well understood in case of E . coli . The Hsps in this organism nearly account to 2% and 20-25% of
the total proteins when grown at 30°C and 46°C, respectively. This metabolic burden is maintained
by the regulatory role of σ 32 (a transcription factor) that is bound to the RNA polymerase (RNAP)
which recognizes the promoters of the heat shock genes so that their transcription and translation
can occur. It means the synthesis, activity and stability of σ 32 constitute important events in signal
perception and transduction of heat shock response. However, in cyanobacteria there are as yet no
evidences for the involvement of any transcription factor that regulates the synthesis of Hsps. A sigma
factor related stress response has been well established in case of B . subtilis also (Yura et al ., 2000;
Dartigalongue et al ., 2001; Helmann et al ., 2001; El-samad et al ., 2005). In addition, several repressor
proteins and their binding sites have been reported. In many of the gram-positive bacteria, HrcA
repressor protein and its binding site CIRCE (for controlling inverted repeat for chaperone expression)
have been reported (Narberhaus, 1999). CIRCE is an inverted repeat consisting of 9 bp separated by
a 9 bp-spacer. The repressor protein HrcA negatively regulates the expression of grpE - dnaK - dnaJ - and
groESL operons in B . subtilis (Hecker et al ., 1996; Narberhaus, 1999). The existence of a CIRCE element
upstream of hrcA gene in B . subtilis signifi es that the hrcA gene is subject to autoregulation. Another
protein, HspR repressor and its binding site HAIR (a cis-element, HSPR-associated inverted repeat)
have been found in Streptomyces coelicolr and Mycobacterium tuberculosis that regulate dnaK operon
and clpB (Stewart et al ., 2002; Bucca et al ., 2003). In B . subtilis , a CtsR system (Derre et al ., 1999) and
the RheR repressor in Streptomyces albus G (Servant et al ., 1999) have been reported.
Webb et al . (1990) fi rst reported a CIRCE element in the 5'-UTR region of groESL operon in S .
elongatus PCC 7942, but the corresponding repressor protein (HrcA) was not described. Nakamoto
et al . (2003) conducted a search of 5'-upstream regions of a number of cyanobacterial groE genes
and found the CIRCE sequence (5'-TTAGACTC-N9-GAGTGC-3') with the exception of S . vulcanus
groEL2 (Furuki et al ., 1996). The transcriptional start sites of groESL1 operons from Synechocystis sp.
strain PCC 6803 and S. elongatus PCC 7942 have transcriptional start sites at the same nucleotide
located within the CIRCE. A search of many cyanobacterial genomes for hrcA gene sequence (http://
www.kazusa.or.jp./cyano/) revealed the presence of hrcA homologues in Synechocystis sp. strain
PCC 6803, T. elongatus BP-1 and Anabaena sp. strain PCC 7120. The deduced amino acid sequence of
HrcA was homologous to the other HrcA proteins. The absence of a CIRCE sequence upstream of
the cyanobacterial hrcA genes indicates that the hrcA is not subject to autoregulation as reported in
case of B . subtilis . In Synechocystis sp. strain PCC 6803, gene sll1670 encodes HrcA and this regulates
the groESL1 operon and the groEL2 gene. The sll1670 gene inactivated mutants of Synechocystis sp.
strain PCC 6803 showed a depression in the activity of groESL1 and groEL2 genes but the expression
of other heat shock genes remained unaffected. The fact that the expression of groESL genes in the
mutant is not completely repressed and the increase in their expression after a heat shock suggests
that there are two different regulatory mechanisms. The fi rst one is a negative regulation governed
by HrcA and a second unknown positive one. Under normal growth conditions, the interaction of