dictyNews
Electronic Edition
Volume 46, number 29
October 23, 2020
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Abstracts
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Polyphosphate is an extracellular signal that can facilitate bacterial
survival in eukaryotic cells
Ramesh Rijal, Louis A. Cadena, Morgan R. Smith, Joseph F. Carr,
and Richard H. Gomer
Department of Biology, Texas A&M University, College Station,
TX 77843-3474 USA
PNAS, accepted
Polyphosphate is a linear chain of phosphate residues and is present
in organisms ranging from bacteria to humans. Pathogens such as
Mycobacterium tuberculosis accumulate polyphosphate, and reduced
expression of the polyphosphate kinase that synthesizes polyphosphate
decreases their survival. How polyphosphate potentiates pathogenicity
is poorly understood. Escherichia coli K-12 do not accumulate
detectable levels of extracellular polyphosphate, and have poor survival
after phagocytosis by Dictyostelium discoideum or human macrophages.
In contrast, Mycobacterium smegmatis and Mycobacterium tuberculosis
accumulate detectable levels of extracellular polyphosphate, and have
relatively better survival after phagocytosis by D. discoideum or
macrophages. Adding extracellular polyphosphate increased E. coli
survival after phagocytosis by D. discoideum and macrophages.
Reducing expression of polyphosphate kinase 1 in M. smegmatis
reduced extracellular polyphosphate and reduced survival in
D. discoideum and macrophages, and this was reversed by the addition
of extracellular polyphosphate. Conversely, treatment of D. discoideum
and macrophages with recombinant yeast exopolyphosphatase reduced
the survival of phagocytosed M. smegmatis or M. tuberculosis.
D. discoideum cells lacking the putative polyphosphate receptor GrlD
had reduced sensitivity to polyphosphate, and compared to wild-type
cells showed increased killing of phagocytosed E. coli and M. smegmatis.
Polyphosphate inhibited phagosome acidification and lysosome activity
in D. discoideum and macrophages, and reduced early endosomal
markers in macrophages. Together, these results suggest that bacterial
polyphosphate potentiates pathogenicity by acting as an extracellular
signal that inhibits phagosome maturation.
submitted by: Ramesh Rijal [[log in to unmask]]
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