Hostile takeover in the cell: Pathogens hijack host mitochondria

Date:
January 14, 2022
Source:
Max Planck Institute for Biology of Ageing
Summary:
A research team reports that a parasite tricks mitochondria into
shedding large structures from their 'skin', thus turning off
their defenses.



FULL STORY ========================================================================== Mitochondria are known as energy suppliers for our cells, but they
also play an important role in the defense against pathogens. They
can initiate immune responses, and deprive pathogens of the nutrients
they need to grow. A research team led by Lena Pernas of the Max Planck Institute for Biology of Ageing in Cologne, Germany, has now shown that pathogens can turn off mitochondrial defense mechanisms by hijacking a
normal cellular response to stress.


==========================================================================
To survive, pathogens need to acquire nutrients from their host and
counter host defenses. One such defense comes from host mitochondria,
which can deprive them of nutrients they need and thus restrict their
growth. "We wanted to know how else mitochondrial behaviour changes when mitochondria and pathogens meet in cells. Because the outer membrane of
these organelles is the first point of contact with the pathogens, we
took a closer look at it," explains Lena Pernas, research group leader
at the Max Planck Institute for Biology of Ageing.

Mitochondria shed their 'skin` The researchers infected cells with the
human parasite Toxoplasma gondii and observed live under the microscope
what happens to the outer compartment of mitochondria. "We saw that mitochondria in contact with the parasite started shedding large
structures from their outer membrane. This was so puzzling to us. Why
would mitochondria shed what is essentially the gateway between them
and the rest of the cell?" says Xianhe Li, first author of the study.

Hostile takeover But how does the parasite get the mitochondria to do
it? The research team was able to show that the pathogen has a protein
that functionally mimics a host mitochondrial protein. It binds to
a receptor on the outer membrane of mitochondria, to gain access
to the machinery that ensures proteins are transported inside the
mitochondria. "In doing so, the parasite hijacks a normal host response
to mitochondrial stress that, in the context of infection, effectively
disarms the mitochondria" Pernas said. "Other researchers have shown
that a SARS-CoV-2 virus protein also binds to this transport receptor.

This suggests the receptor plays an important role in the host-pathogen interaction. But further investigation is needed to better understand its
role during different infections." Lena Pernas is also a group leader
at the CECAD Cluster of Excellence in Aging Research at the University
of Cologne.

========================================================================== Story Source: Materials provided by
Max_Planck_Institute_for_Biology_of_Ageing. Note: Content may be edited
for style and length.


========================================================================== Journal Reference:
1. Xianhe Li, Julian Straub, Ta^nia Catarina Medeiros, Chahat Mehra,
Fabian
den Brave, Esra Peker, Ilian Atanassov, Katharina Stillger, Jonas
Benjamin Michaelis, Emma Burbridge, Colin Adrain, Christian Mu"nch,
Jan Riemer, Thomas Becker, Lena F. Pernas. Mitochondria shed their
outer membrane in response to infection-induced stress. Science,
2022; 375 (6577) DOI: 10.1126/science.abi4343 ==========================================================================

Link to news story: https://www.sciencedaily.com/releases/2022/01/220114092821.htm

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