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CYTOSKELETAL

ORGANIZATION AND
DYNAMICS By: Cristina L. Amarante
Msc, Advanced of Cells and Molecular Biology
Master of Science in Biology, University of the Southern Philippines
Objectives
• Define cytoskeleton
• Compare and contrast actin filaments, microtubules and intermediate
filaments
• Supplement additional articles that could prove the cytoskeleton
functions and dynamics.
The Cytoskeleton
1. Intermediate Filaments (Ifs)
Intermediate Filaments
• Common structure:
• assembly
Filaments (IFs)
2. Microtubules
3. Microfilament (MFs) / Actin
microfilaments
Actin
Literature Reviews in relation to
the cytoskeleton organization
and dynamics.
Faulty cytoskeleton impairs immune cells
Crucial factor for adaptive immunity discovered in rare disease

Date:
July 26, 2018
Source:
CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences
Summary:
The rearrangement of the cell´s inner scaffold, the cytoskeleton, is a vital process for immune
cells. In a new collaborative study, a rare inherited disease revealed a hitherto unknown role of
a cytoskeleton-regulating factor for the proper functioning of the adaptive immune system.
Faulty cytoskeleton impairs immune cells
Crucial factor for adaptive immunity discovered in
rare disease
• Background : The cytoskeleton composed of actin filaments is crucial for every active movement
of a cell. By rearranging these filaments, cells can stretch and wander in every direction, squeeze
into the smallest gaps or wrap themselves around an object. Defects of the cytoskeleton thus can
have detrimental effects on the immune response and thereby on the ability of the organism to
control infections.
• Methods : The gene defect was found in six patients who presented with severe infections of the lung,
skin and oral mucosa. Genetic analyses of their genomes revealed mutations in a gene for a protein called
WDR1, an important factor for the turn-over of actin filaments and thereby the dynamic remodeling of the
cytoskeleton.
• Results: Through a series of extensive analyses, the researchers found that WDR1 deficiency leads to
aberrant T-cell activation and B-cell development.
• Conclusion: Our study identifies a novel role for WDR1 in adaptive immunity, highlighting WDR1 as a central
regulator of actin turnover during formation of the B-cell and T-cell immunologic synapses.
• Reflection: The results allowed the researchers to gain new insights into the key role of actin cytoskeletal
dynamics in supporting immune cell function. This study is another example for the value of research on rare
diseases -- not only for the few affected patients, but for a more global and fundamental understanding of
human biology.
Seafood poisoning bug thwarts a key host
defense by attacking the cell’s cytoskeleton
Date: June 22, 2017
Source: UT Southwestern Medical Center
Summary:
This study identifies the virulence factor used by V. parahaemolyticus
to suppress host ROS generation and also reveals an unprecedented
mechanism used nu a microbial pathogen to do so.
Seafood poisoning bug thwarts a key host
defense by attacking the cell’s cytoskeleton
• Background: Without a working cytoskeleton, infected cells are unable to produce
defensive molecules called reactive oxygen species (ROS) that normally attack bacterial
DNA. Vibrio parahaemolyticus bacteria deploy a needlelike apparatus called a Type III
Secretion System (T3SS) that injects toxic bacterial proteins, known as effectors, into
cells that line the intestine, resulting in severe gastroenteritis.
• Methods: The researchers created two V. parahaemolyticus strains, one able to make
VopL and another not. Using confocal microscopy, they found that the Vibrio able to
produce VopL inactivated the assembly of ROS by gathering the cytoskeleton into
nonfunctional filaments. In contrast, the mutant bacterium unable to produce VopL was
vulnerable to ROS attack.
• Results: The researchers found that, one of One of V. parahaemolyticus' many effectors --
VopL -- paralyzes the cytoskeleton through a novel mechanism.
• Reflection: By hijacking the cytoskeleton, VopL prevents the cell from launching one of its
major weapons, reactive oxygen species.

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