L6- Pathogens and immunity Flashcards
what does agrobacterium tumefaciens do to plants
agrobacterium tumefaciens has a Ti plasmid that reprograms the host, this can be exploited
part of the plasmid is transferred to the plant (T-DNA=transfer DNA), the T-DNA encodes genes that are active in the plant to
- produce high levels of auxin and cytokinin
-produce high levels of opine sugars
-auxins also suppress SA-mediated defence
as high auxins and cytokinins promote cell division and make the plant produce many undifferentiated cells (callus), high auxins suppress defence responses- developing gall acts as a strong sink for carbs and novel sugars are formed
rest of the plasmid contain genes
-enabling the bacterium to metabolise opine sugars
-enabling the DNA transfer to the host
-allowing plasmid replication and transfer between bacteria (conjugation)
what does Rhodococcus facians do to plants
R.facians virulence genes are encoded on a linear plasmid
early part of lifecycle is endophytic (lives in plant cell), the att (attenution) genes direct the synthesis of a quorum-sensing molecule (modified amino acid), regulated by C and N status of the host, as these change, the att genes are activated and cause a positive feedback loop
fas (fasciation) genes are induced when cell gets crowded - this induce shoot-inducing cytokinin synthesis genes
does not involve auxin
how do cytokinins work?
they are complex, CK precursors activate CKs at certain time, then it activates it, but also need to be degraded
three types of CK
iP, tZ, cZ
these are detected by receptors 3 types (AHK2, AHK3, AHK4)- leading to CK response of defence or cell proliferation
two routes for synthesis
IPTs (isopentenyl tranferases) synthesise CK precurses from Dimethylallylpyrophosphate and adenine, adenine can come from AMP/ADP/ATP or tRNA
-route 1= synthesises isopentenyl adenine (iP) and trans-zeatin (tZ)
-route 2= synthesises cis zeatin(cZ)
What is the relationship between R.Fascians and cytokinins
r.fascians make multiple CKs, iP, cZ,tZ, unusual CKs (methyl derivates)
methylated CKs are active, ARR5 and ARR6 gene expression is induced bycytokinin, iP induces over umolar range
thr CK ratios change during the course of infection, tZ fall, iP rises MeIP rises = methyl IP is really resistant to degradation (this means dont need to make much)
pathogenic CKS tend to preferentially activate AHK3, AHK4 leading to cell proliferation (and supress defence responses)
AHK4 expression is induced to tissue sensitivity to CK increases
MeiPs are resistant to degradation so cells , hyper-proliferate as CK content is high, plant derived CKs tend to reduce, particularly tZ, tZ binds preferentially to AHK2 (which leads to defence reactions)
by altering the iP/tZ ratio the pathogen pushes the plant towards susceptibility and away from resistance
what is overview of what R.facians do
stimulate cell proliferation, make leafy gall, repress defence response does so by increasing CKs but also changing host sensitivity and the CK mixture
what do root knot nematodes and cyst nematodes do to plant development
many type of pathogenic nematodes, some pentrate via root tip, other directly. They feed via a stylet but change host development to make giant feeding cells or syncitia
nematodes manipulate host development in numerous ways
cyst- manupulation of auxin signalling
heterodera schachtii produce effector that binds to the auxin influx protein LAX3, leads to increased auxin influx and cell expansion, redirects auxin to lateral cells via PIN1
RKN- manipulation of metabolism
meloidogyne javanica produce a secreted chorismite synthase , this has no role in animals but is important in plants producing salicylic acid and phytoalexins
RKN- manipulation of cell walls
globodera rosochiensis produces an expansion that modifies cell wall expansion
RKN- manipulation of development
heterodera glycines and heterodera schachii produce peptide signalling molecules (CLE-like), these play a central role in controlling meristem activity and cell fate
