PAMP Signaling in Plant Innate Immunity - PAMP Signals in Plant Innate Immunity: Signal Perception and Transduction - page 77

function to a certain extent, while loss of CRT3 alone abrogates EFR function
completely, suggesting that CRT3 contributes more to the ER-QC function than the
other two CRT genes (Li et al. 2009b ). CRT3 has been show n to be an ER-localized
protein and it is required for EFR protein accumulation (Li et al. 2009b ). A crt3 null
mutant did not accumulate EFR protein, suggesting that EFR is a substrate for CRT3
(Li et al. 2009b ). The Erd2b mutant did not accumulate CRT3 protein. ERD2B seems
to be HDEL receptor for CRT3 that allows its retro-translocation from the Golgi to
the ER (Li et al. 2009b ). The crt3 mutants were more susceptible to P . syringae pv.
tomato strains than efr mutants. It suggests that EFR is not the only PRR whose func-
tion is compromised by CRT3 mutations (Li et al. 2009b ).
Nekrasov et al. ( 2009 ) have demonstrated the requirement of the soluble luminal
protein Hsp40 ERdj3 for elf18 responses. ERDj3B is an ER-localized member of
the HSP40 co-chaperone family. Arabidopsis erdj3b-1 mutant plants were strongly
affected in the bacterial PAMP elf18-triggered oxidative burst and MAP kinase acti-
vation (Nekrasov et al. 2009 ). SDF2 has also been shown to be required for EFR
biogenesis (Nekrasov et al. 2009 ). Sdf2 mutants are strongly impaired in EFR pro-
tein accumulation. The sdf2 mutant plants were strongly affected in the PAMP
elf18-triggered oxidative burst and MAP kinase activation. Loss of SDF2 results in
ER retention and degradation of EFR (Nekrasov et al. 2009 ). However, the sdf2 or
erdj3b mutants are not completely insensitive to elf18, suggesting that BiP retention
is less critical than CRT-based ER-QC for EFR proper folding and protein accumu-
lation (Nekrasov et al. 2009 ).
SDF2 exists in a complex with ERdj3B and BiP3, in which ERdj3B may act as
a bridge between SDF2 and BiP-3. As both SDF2 and ERdj3B lack an ER reten-
tion signal, their ER localisation might be due to interaction with BiPs (Nekrasov
et al. 2009 ). BiP and CRT exist in an abundant large complex in tobacco (Crofts
et al. 1998 ). CRT3, SDF2, Erdj3B, BiP, and potentially UGGT may exist in the
same complex to regulate proper EFR folding (Li et al. 2009b ). EFR biogenesis
may require the SDF2/ERdj3B/BiP complex, in addition to ER-QC mediated by
CRT3 and UGGT.
The other lectin component calnexin has been shown to be not necessary for
biogenesis of EFR. A double mutant in two calnexin genes, CNX1 and CNX2
showed no impairment in elf18-triggered oxidative burst, or defense gene induction
(Li et al. 2009b ). These results suggest that calnexins may not be involved in the
biogenesis of EFR.

2.17.6 ER Quality Control Components Required

for Biogenesis of the PRR FLS2

The differential requirement of EFR and FLS2 for ER-QC and glycosylation com-
ponents has been reported (Nekrasov et al. 2009 ). Both crt3 and uggt mutants were
unaltered in oxidative burst triggered by fl g22, suggesting that UGGT and CTR may