Biology Reference
In-Depth Information
and 2 x 10
5
copies in the month of July. These numbers are considered to be higher by about 200
times the cell number determined by microscopy. This has been explained on the basis that the cells
of
Microcystis
contain several copies of
mcyA
gene (up to a maximum of 11) during the transition
from the logarithmic growth phase to the stationary phase. However, a positive correlation existed
between the total microcystin concentration and the copy number of the
M
.
aeruginosa
mcyA
gene
(Kurmayer and Kutzenberg, 2003; Yoshida
et al
., 2005, 2007). A change in the toxin-producing sub-
population of
M
.
aeruginosa
was noted over a period of time with the growth of non-toxic strains
outcompeting in summer. The cyanophage abundance was negatively correlated with the abundance
of
M
.
aeruginosa
. During summer, when cyanophage abundance increased, a simultaneous decline in
the host population was noted. So a seasonal shift in the composition of the different sub-populations
of
M
.
aeruginosa
was evident. On the basis of phylogenetic classifi cation of the
g91
sequence analysis,
a number of genotypes (a to j) of cyanophages have been noted during the period of study with
genotype 'a' being most frequently represented in Lake Mikata. This sequence appeared to be
identical to the sequences of Ma-LMM01, Ma-LMM02, Ma-LMM03 and Ma-LMM05 that are specifi c
to only microcystin-producing populations of
M
.
aeruginosa
(Yoshida
et al
., 2006; Takashima
et al
.,
2007; Yoshida
et al
., 2008). Although genotypes 'b' to 'j' were represented only once, they had 98.9%
identity to genotype 'a'. It is concluded that the cyanophage assemblage has the ability to kill only a
small proportion of
M
.
aeruginosa
population paving the way for the replacement of phage-sensitive
population by phage-insensitive population. The present understanding is that viruses will infect
the most abundant host species because of high encounter rates and “killing the winner” viruses
maintain the coexistence of competing species, a hypothesis proposed earlier by Thingstad and
Lignell (1997). To quantify cyanophage Ma-LMM01 infected cells in the natural populations of
M
.
aeruginosa
, Yoshida
et al.
(2010) detected
g91
(RNA polymerase B) gene transcripts. Based on the
relative abundance of
g91
gene transcripts before onset of release of virus progeny in the culture
based experiments, it was feasible to assay of transcripts of
g91
in the infected cells under natural
conditions by real-time reverse transcription PCR. The levels of expression of
g91
(10
-2
per
rnpB
transcript) in natural waters corresponded with the expression levels in cultures.
X. MUTATIONAL STUDIES ON FRESHWATER CYANOPHAGES
Plaque-type, host-range and conditional lethal mutants have been isolated and characterized.
Spontaneous mutants of LPP-1 exhibiting unstable rapid lysis (
r
) character were described by
Safferman and Morris (1964b). Singh
et al.
(1972) characterized stable
r
mutants of LPP-1 in addition
to minute, host-range (
h
) and acrifl avine-resistant mutants. Rimon and Oppenheim (1975) isolated
nitrosoguanidine (MNNG)-induced temperature-sensitive (
ts
) mutants of LPP-2 SP-1 who showed
complementation and recombination among these mutants. Singh and Chaubey (1976) reported the
induction r-mutants with hydroxylamine. Singh and Kashyap (1976) conducted a detailed study
on induction of
h
and
ts
markers in LPP-1 after mutagenesis with MNNG and 2-aminopurine and
suggested that these represented point mutations. Amla (1979, 1981) reported
h
and minute plaque-
forming mutants of phage AS-1 whereas AS-1 resistant mutants of
A
.
nidulans
were reported by Bisen
et al
. (1985). Cyanophage LPP-1 resistant mutants of
P
.
uncinatum
were subsequently isolated and
characterized (Bisen
et al
., 1986b). The isolation and characterization of host-range mutants (Sarma
and Kaur, 1993, 1997) and temperature-sensitive mutants of cyanophage N-1 (Sarma and Singh,
1994, 1995) were reported for the fi rst time. The development of cyanophage N-1 has been studied
under the stress of heavy metals (Sarma and Kaur, 2005).
