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The Wolbachia WalE1 effector alters Drosophila endocytosis
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Abstract
The most common intracellular bacterial infection is
Wolbachia pipientis
, a microbe that manipulates host reproduction and is used in control of insect vectors. Phenotypes induced by
Wolbachia
have been studied for decades and range from sperm-egg incompatibility to male killing. How
Wolbachia
alters host biology is less well understood. Previously, we characterized the first
Wolbachia
effector – WalE1, which encodes a synuclein domain at the N terminus. Purified WalE1 sediments with and bundles actin and when heterologously expressed in flies, increases
Wolbachia
titer in the developing oocyte. In this work, we first identify the native expression WalE1 by
Wolbachia
infecting both fly cells and whole animals. WalE1 appears as aggregates, separate from
Wolbachia
cells. We next show that WalE1 co-immunoprecipitates with the host protein Past1 and that WalE1 manipulates host endocytosis. Yeast expressing WalE1 show deficiency in uptake of FM4-64 dye, and flies harboring mutations in
Past1
or overexpressing WalE1 are sensitive to AgNO
3
, a hallmark of endocytosis defects. Finally, we also show that
Past1
null flies harbor more
Wolbachia
overall and in late egg chambers. Our results identify interactions between a
Wolbachia
secreted effector and a host protein and point to yet another important host cell process impinged upon by
Wolbachia
.
Title: The
Wolbachia
WalE1 effector alters
Drosophila
endocytosis
Description:
Abstract
The most common intracellular bacterial infection is
Wolbachia pipientis
, a microbe that manipulates host reproduction and is used in control of insect vectors.
Phenotypes induced by
Wolbachia
have been studied for decades and range from sperm-egg incompatibility to male killing.
How
Wolbachia
alters host biology is less well understood.
Previously, we characterized the first
Wolbachia
effector – WalE1, which encodes a synuclein domain at the N terminus.
Purified WalE1 sediments with and bundles actin and when heterologously expressed in flies, increases
Wolbachia
titer in the developing oocyte.
In this work, we first identify the native expression WalE1 by
Wolbachia
infecting both fly cells and whole animals.
WalE1 appears as aggregates, separate from
Wolbachia
cells.
We next show that WalE1 co-immunoprecipitates with the host protein Past1 and that WalE1 manipulates host endocytosis.
Yeast expressing WalE1 show deficiency in uptake of FM4-64 dye, and flies harboring mutations in
Past1
or overexpressing WalE1 are sensitive to AgNO
3
, a hallmark of endocytosis defects.
Finally, we also show that
Past1
null flies harbor more
Wolbachia
overall and in late egg chambers.
Our results identify interactions between a
Wolbachia
secreted effector and a host protein and point to yet another important host cell process impinged upon by
Wolbachia
.
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