Plants and animals alike fall sick
when infected by something pathogenic: viruses, bacteria, oomycetes, and more.
Thankfully, higher-order eukaryotes have evolved multiple ways to stop many of
these bugs from “taking over”. However, these mini critters don’t give up quite
so easily, and have a few clever tricks of their own to combat the host immune
system. This paper investigates the strategy of RNA silencing suppressors, a
counter defense utilized by the Phytophthora
microbial plant pathogens.
Before
discussing the paper, however, why bother to study this topic? First of all,
humans rely on plants for everyday life. If one understands the ways this group
of notorious crop pathogens causes plant sickness, we will have an edge in
curbing the economical and physical damage caused by these microbes to the
supply of food worldwide. For example, in Ireland, the potato famine was caused
by
Phytophthora infestans; since 1845, the pest causes endemic loss
of crop of up to 50% seven out of ten years (1). More importantly,
however, we will have a model that may be extrapolated to other critical plant
species and even animals when trying to tailor specific cures for diseases in
the future. As with all science, understanding a little piece of the puzzle has
multifaceted usefulness, because often this piece can help us solve the puzzles
in other plants and animals. This paper successfully characterizes factors in Phytophthora plant pathogens that
contribute to its successful virulence in the hopes of demonstrating that
further characterizations of factors in relevant organisms will help in finding
effective cures.
One method
by which a host may prevent, or at least lessen, the infection of pathogens,
especially against RNA viruses, is to encode for miRNAs or siRNAs; small-RNAs
that work to degrade the genetic material of the invading species (2). But what
happens when Phytophthora creates
something called an effector, a factor boosting virus fitness (3) where the
small-RNA defense mechanism is actually disabled? You get successful infection
of the invading species, or at least enhanced succeptibility. In a series of
clever experiments, Qiao et al. characterized PSR1 and PSR2, miRNA/siRNA
interfering proteins of pathogens belonging to the Phytophthora genus.
As can be
seen in Figure 1, the authors’ first experiment demonstrated that the RNA
silencing defense system is interrupted in the leaves of N. benthamiana when infected with a PSR-containing version of Agrobacterium tumefaciens, which was designed
to express GFP. Agrobacterium tumefaciens
is a soil bacterium that causes tumors in plants when introduced into a plant
(4). Normally, the plant’s small-RNA defense system would destroy the invader,
disallowing it to express GFP. However, when coexpressed with the effectors,
high levels of fluorescence were observed, suggesting that these effectors were
disabling the plant’s small-RNA immune response. They also showed that PSR1
effectors might have an amplified immune-system suppression effect (systemic
silencing); this places an even greater stress on trying to characterize these elements,
as they may be key factors in the pathogenesis of particular invaders.
The authors
also demonstrated in Figure 2 that PSR1 is affecting the biogenesis of siRNAs
and miRNAs, not their activity. Since bugs expressing the PSR1 (versus the
control, which was not) caused levels of pre-miRNA to drop but not pri-miRNA
levels, and because pre-miRNAs are derived by processing of pri-miRNAs via DCL1
(which is also responsible in part for the biogenesis of siRNAs and miRNAs),
the differential abundance suggests that the PSR1 is interacting with DCL1 and
preventing pre-miRNA synthesis which is also interrupting small-RNA biogenesis.
This finding is valuable: it provides information on the type of mechanism for
getting around the host defenses. Many VSRs (viral suppressors of RNA
silencing) actually operate by binding to directly to small-RNAs (CITATION),
but by knowing where in the pathway host defenses are failing, it will make a
targeted cure far more effective. Further, the authors showed that PSR2 does
not affect small-RNA biogenesis, but rather, plays a role in the block of other
host-defense genes. This shows that the two effectors are likely working in
tandem to promote infection. Figures 3, 4, and 5 were experiments separate from
1 and 2, designed to further support the hypothesis that the PSR1 and PSR2 are
important for the promotion of Phytophthora
pathogenesis.
What is
important to understand from this paper is not necessarily what PSR1 and PSR2
effectors do, but rather understand the importance of characterizing such
effectors. By having a better grasp on understanding what is responsible for
thwarting our bodies’ defenses, steps may be taken to research potential ways
to disable these invaders’ virulence strategies. This paper is a fundamental
step in moving towards clinical solutions for ailed mammals as well as in
plants ravaged by these pathogens.
Primary article:
Supporting
articles:
1) Dowley L,
Grant J, Griffin D. (2008) Yield losses
caused by late blight (Phytophthora infestans (Mont.) de Bary) in potato
crops in Ireland.
Irish Journal of Agricultural
and Food Research 47: 69–78
3) Jones J, Dangl J. (2006) The plant immune system. Nature. doi:10.1038/nature05286
4) Hoekema A, Hirsch P,
Hooykaas P, Schilperoort R. (1983) A
binary plant vector strategy based on separation of vir- and T-region of
the Agrobacterium tumefaciens Ti-plasmid. Nature. doi:10.1038/303179a0
5) Burgyán J, Havelda Z. Viral suppressors of RNA silencing. Cell. Volume 16, Issue 5, May 2011,
Pages 265–272
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