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A decrease in CO 2 fi xation rate was noted in Plectonema as a result of LPP-1 infection and
this closely corresponded with the invagination of the photosynthetic lamellae. It is in this area
that the newly synthesized virions accumulated (Sherman and Haselkon, 1970a,b). Sherman and
Haselkorn (1971) observed that DCMU had little effect on LPP-1 multiplication except that it
decreased the burst size. This modest decrease in burst size was attributed to the lowering of cyclic
photophosphorylation relative to non-cyclic type. Padan et al . (1971b) showed that LPP-1G is a
thermosensitive cyanophage, since the development is inhibited at 35°C. This is explained due to
the cessation of CO 2 photoassimilation as well as invagination of photosynthetic lamellae.
Mackenzie and Haselkorn (1972c) have shown that for the synthesis of SM-1 phage, photosynthetic
metabolism of the host is essential since withdrawl of CO 2 or of light completely suppressed viral
growth. Moreover, the incorporation of DCMU or CCCP also suppressed viral growth. Adolph and
Haselkorn (1972) reported similar observations after N-1 infection.
The development of phage progeny of AS-1M in S . cedrorum requires the photosynthetic
machinery intact, since phage development did not occur when photosynthesis was inhibited by
DCMU, CCCP, valinomycin, nigericin or lack of CO 2 . However, supplementation of glucose in dark
or in light with DCMU (10 -5 M) supported phage production to about 10% of control (Sherman, 1976).
Synthesis of cyanophages A-1(L) and A-4(L) did not occur in darkness but illumination, though for
brief periods, supported reduced phage burst. The presence of DCMU and dinitrophenol did not
inhibit their development in light (Al-Musavi, 1977).
Amla (1979) compared intracellular development of phage AS-1 in two pigment mutants,
i.e. blue and yellow of A . nidulans . Phage AS-1 development was subjected to DCMU-mediated
inhibition in the cells of blue mutant similar to that of parent strain. Whereas in the cells of the yellow
mutant, phage multiplication was slow with reduced yield. Cyanophage AS-1 infection caused
signifi cant changes in the structure of photosynthetic apparatus. PSI reaction centre was the most
resistant to degeneration (Gusev et al ., 1980a). Gusev et al . (1980b) employed ESR, luminescence and
polarography methods to identify the specifi c reaction centre in the photosynthetic apparatus of
A . variabilis infected by cyanophage A-1(L). The virus fi rst showed disturbance in the functioning
of PSII followed by alterations in the thylakoid arrangement. Mamkayeva et al . (1980) observed
the maturation of A-1(L) cyanophages in A . variabilis in an electron transparent local zone near or
between thylakoids in cells exposed to DCMU (5 x 10 -6 M). Photosynthetic inhibitors and removal
of light suppressed the replication of SM-2 suggesting that it is dependent on host's photosynthetic
metabolism for energy required for replication (Benson and Martin, 1981). Cyanophage SM-2 has
also been reported to be highly dependent for its development on photosynthetic metabolism of
the host cells (Benson and Martin, 1981). Amla and Saxena (1983) described the metabolic aspects
of cyanophage AS-1 replication in A . nidulans . Viral multiplication did not occur in dark and the
latent period was prolonged when the infected cells of A . nidulans were in dark for 6 h followed by
illumination in presence of CCCP and DCMU. Phage growth was abolished due to chloramphenicol
treatment whereas treatment with rifampicin and actinomycin-D before eclipse period abolished
AS-1 development. While majority of the evidences presented above substantiate photosynthesis-
dependent cyanophage multiplication cycle, Bisen et al . (1988) reported that LPP-1 multiplication
cycle in Phormidium uncinatum does not depend on photosynthesis.
Cyanophage N-1 infected cells of N . muscorum supported virus development in the absence of
PSII activity and energy for phage multiplication is provided by cyclic photophosphorylation as
well as via a degradation of carbohydrate reserves (Kashyap and Singh, 1989). Cyanophage infection
not only inhibited PSII activity at the level of secondary acceptor, Q(B) of PSII but also D1 protein
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