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TABLE 15.2 T3SS effectors of Shigella —cont'd
Number of T3SS effectors present in each
genome a
Interacting
proteins/
enzymatic targets
Homolog (EPEC/
EHEC homologs in
bold)
S. dysenteriae
Sd197
300267
S. flexneri
Sf301
198214
S. boydii
Sb512
344609
S. sonnei
Ss046
300269
Effector
Function
OspI
Immunomodulation -
reduces NF κ B by
deamidating UBC13
UBc13 ( Sanada et al.,
2012 )
-
1
1
1
1
OspZ
Immunomodulation -
disrupts NF κ B signaling,
reduces PMN migration
-
NleE
1
1
1
1
IpaH ( plasmid)
Immunomodulation -
blocks NF κ B activation by
E3 ubiquitin ligase activity
NEMO/IKK γ , ABIN-1
( Ashida et al., 2010 )
E2 Ub ligases
(UBE2D1, UBE2D3
and UBE2D4) ( Singer
et al., 2008 )
SspH
5
5
4
4
IpaH
( chromosomal)
Potentially immunomodu-
lation - E3 ubiquitin ligase
-
SspH
5(1)
4(3)
5
5
a Effectors were identified by tBlastN searches using Integrated Microbial Genomes (DOE Joint Genome Institute).
b Numbers in brackets indicate pseudogenes present in genome which may occur through frameshifts, internal deletions, internal stop codons, N-terminal or C-terminal
truncations, absent start codons, etc. Importantly, while some of these pseudogenes have been confirmed, others may be the result of sequencing errors (the effector may
still be translocated and functional), and some mutations (e.g. internal or C-terminal deletions) may still result in a translocated and potentially functional effector.
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