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the regulation of Hik34-Rre1 system. Genes of Group 3 essentially (those of unkown function
sll0939 and slr 0967) include those that were not affected due to mutation of Hik33 and Hik34 but
were suppressed to basal levels of function in Hik16 and Hik41 mutant cells. The genes included
in Group 4 are those whose induction of expression was unaffected by inactivation of any of the
examined Hiks. Genes such as rlpA and repA (for rare lipoprotein A), htrA (for a serine protease)
and 17 other genes belong to this category. A screening of gene knock-out libraries of Synechocystis
sp. strain PCC 6803 for Hiks and Rres governing hyperosmotic stress revealed that 32 of the 52
hyperosmotic stress-inducible genes are under the control of Hik33, Hik34 or Hik16 and Hik41.
However, the rest 20 genes induced by hyperosmotic stress are under the regulation of some other
unknown mechanism(s). Moreover, the observations of Kanesaki et al . (2002) that there are special
type of genes that are expressed under salt stress ( pbp gene for penicillin-binding protein and ctpA
gene for C-terminal processing protease) and hyperosmotic stress ( fabG, rlpA, repA ) are worth
mentioning. Though there are similar kinds of Hiks operating under salt and hyperosmotic stress,
the types of genes expressed under their control differ in the two stresses (Paithoonrangsarid et
al ., 2004). This has further been confi rmed by the screening of the gene knockout libraries of Rres
by RNA slot-blot hybridization followed by a genome-wide DNA microarray (Shoumskaya et al .,
2005). In addition to Hik33, Hik34, Hik16 plus Hik41, Hik10 is also involved in the perception of
salt stress and such signals are received by the Rre31, Rre17, Rre1 and Rre3. These thus regulate the
expression of a large number of genes. The recognition of Hik33-Rre31, Hik34 or unidentifi ed Hik-
Rre1, Hik10-Rre3 and Hik16-Hik41-Rre17 systems function to perceive and transduce the signals of
both salt and hyperosmotic stress as reported earlier (Paithoonrangsarid et al ., 2004). A single gene
( htrA gene in case of Hik10-Rre3 system) or few genes ( sll0939 , slr0967 and sll0938 in case of Hik16-
Hik41-Rre17 system) were induced in both salt and hyperosmotic stress. In contrast, in case of systems
like Hik33-Rre31 and Hik34-Rre1 and unidentidfi ed Hik-Rre1 the expression of a group of genes
was induced by salt-stress or hyperosmotic stress. Murata and Suzuki (2006) reviewed the utility
of genome sequence of Synechocystis sp. strain PCC 6803 in understanding as to how cyanobacteria
sense environmental stress. By performing targeted mutagenesis of 44 out of 47 Hiks and 42 out
of 45 Rres, the mutant libraries were screened by genome-wide microarray analysis and slot-blot
hybridization. They identifi ed Hiks specifi c for low temperature, hyperosmotic and salt stress and
manganese defi ciency that perceive and transmit signals. Some of the genes for heat shock proteins
( hspA , dnaK2 , dnaJ , groEL2 , clpB1 and clpC ), GG synthesis ( ggpS , glpD ), sigD and hliA appear to be
induced commonly in response to salt-stress and osmotic stress.
Of the seven Spks identifi ed in Synechocystis sp. strain PCC 6803 (SpkA to SpkG), the relative
expression of SpkC, SpkD, SpkF and SpkG has been examined under seven stress conditions (Liang
et al ., 2011). Signifi cantly under high salt conditions SpkG gene is overexpressed when compared to
control cultures and those derived from low and high temperatures and media defi cient in carbon,
nitrogen and phosphorus (Fig. 9). The transcriptional dynamics of these four genes based on
semiquantitative RT-PCR showed that in the salt-stressed cells of Synechocystis sp. strain PCC 6803 the
expression of SpkG is up-regulated while at the same time SpkC is down-regulated. However, in all
other six conditions SpkG is down-regulated but SpkC is up-regulated in all conditions except in high
salt condition. Construction of deletion mutants of SpkC and SpkG and their growth characteristics
under high salt conditions have been helpful in identifying SpkG that plays an important role in
perceiving high salt signal directly. Genome-wide patterns of transcription of genes in the wild-type
and SpkG mutant have been compared by DNA microarray analysis (Fig. 10).
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