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2015 ; 35
(17
): 2932-46
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Salmonella Engages Host MicroRNAs To Modulate SUMOylation: a New Arsenal for
Intracellular Survival
#MMPMID26100020
Verma S
; Mohapatra G
; Ahmad SM
; Rana S
; Jain S
; Khalsa JK
; Srikanth CV
Mol Cell Biol
2015[Sep]; 35
(17
): 2932-46
PMID26100020
show ga
Posttranslational modifications (PTMs) can alter many fundamental properties of a
protein. One or combinations of them have been known to regulate the dynamics of
many cellular pathways and consequently regulate all vital processes.
Understandably, pathogens have evolved sophisticated strategies to subvert these
mechanisms to achieve instantaneous control over host functions. Here, we present
the first report of modulation by intestinal pathogen Salmonella enterica serovar
Typhimurium (S. Typhimurium) of host SUMOylation, a PTM pathway central to all
fundamental cellular processes. Both in cell culture and in a mouse model, we
observed that S. Typhimurium infection led to a dynamic SUMO-conjugated proteome
alteration. The intracellular survival of S. Typhimurium was dependent on SUMO
status as revealed by reduced infection and Salmonella-induced filaments (SIFs)
in SUMO-upregulated cells. S. Typhimurium-dependent SUMO modulation was seen as a
result of depletion of crucial SUMO pathway enzymes Ubc-9 and PIAS1, at both the
protein and the transcript levels. Mechanistically, depletion of Ubc-9 relied on
upregulation of small noncoding RNAs miR30c and miR30e during S. Typhimurium
infection. This was necessary and sufficient for both down-modulation of Ubc-9
and a successful infection. Thus, we demonstrate a novel strategy of
pathogen-mediated perturbation of host SUMOylation, an integral mechanism
underlying S. Typhimurium infection and intracellular survival.
|Animals
[MESH]
|Cell Line, Tumor
[MESH]
|Female
[MESH]
|HeLa Cells
[MESH]
|Host-Pathogen Interactions
[MESH]
|Humans
[MESH]
|Mice
[MESH]
|Mice, Inbred C57BL
[MESH]
|MicroRNAs/*genetics
[MESH]
|Protein Inhibitors of Activated STAT/*metabolism
[MESH]
free
free
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