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Printable Handouts
Navigable Slide Index
- Introduction
- Overview
- The ageing process
- Molecular damage
- The model organism: Caenorhabditis elegans
- C. elegans life cycle
- C. elegans anatomy and development
- C. elegans nervous system
- Key proteins conserved in C. elegans and humans
- Determinants of C. elegans ageing
- C. elegans lifespan plasticity
- Ageing and mitochondrial content
- Diseases with impaired mitochondrial homeostasis
- Mitochondria accumulation during ageing
- No mitochondria accumulated in long-lived mutants
- Mitochondria accumulation & ageing (cause\effect)
- Manipulating mitochondrial content during ageing
- Mitochondrial content impacts lifespan
- Mitochondria accumulation in ageing (mechanism)
- Autophagy and the removal of mitochondria
- Mitophagy paradigms
- DCT-1- the C. elegans Nix/BNIP3 homolog
- Mitophagy mediators
- DCT-1 localized to outer mitochondrial membrane
- Monitoring mitophagy in vivo
- DCT-1 requirement for mitophagy
- PINK-1 requirement for mitophagy
- DCT-1 is a putative mediator of mitophagy
- Mitophagy is required when insulin/IGF-1 are low
- Mitophagy is required under dietary restriction
- Mitophagy deficiency in mitochondrial mutants
- Increased mass upon mitophagy inhibition
- Mitochondria in mitophagy deficient neurons
- Disorganized & fragmented mitochondrial network
- Elevated H2O2 upon inhibition of mitophagy
- Mitophagy deficiency increases cytoplasmic Ca2+
- Mitochondrial depolarization in mitophagy mutants
- Consequences of mitophagy downregulation
- Mitophagy deficiency lowers resistant to stress
- Dopaminergic neurons affected by mitophagy
- Consequences of mitophagy impairment
- The retrograde response
- SKN-1 is activated in mitophagy-deficient worms
- Mitochondrial genes are regulated by SKN-1
- dct-1 expression regulation (DAF-16 & SKN-1)
- SKN-1 requirement for mitophagy
- SKN-1 depletion impairs mitochondrial biogenesis
- SKN-1 compensates for reduced basal mitophagy
- A mitochondrial homeostasis network
- Summary of the talk
- Credits
Topics Covered
- The phenomenon of ageing
- Introducing Caenorhabditis elegans
- C. elegans biology and ageing: features and advantages
- Key discoveries and milestones
- An example: mitochondrial turnover and ageing
Talk Citation
Tavernarakis, N. (2017, January 30). Caenorhabditis elegans: a platform for accelerating research on ageing [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved November 21, 2024, from https://doi.org/10.69645/VPFN2555.Export Citation (RIS)
Publication History
Financial Disclosures
- Prof. Nektarios Tavernarakis has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.
Other Talks in the Series: Aging
Transcript
Please wait while the transcript is being prepared...
0:00
Hello,
and welcome to this presentation
on the use of the nematode worms Caenorhabditis elegans
in ageing research.
My name is Nektarios Tavernarakis.
I'm a Professor at the University
of Crete Medical School,
and a Research Director
at the Foundation
for Research and Technology
in Heraklion, Crete, Greece.
0:20
I will begin by introducing
and defining
the phenomenon of ageing,
in relation to biological systems.
I will then introduce
Caenorhabditis elegans,
focusing primarily on its biology,
features and advantages
relevant to ageing research.
In the following part of the talk,
I will give you an overview
of the main factors
and mechanisms
that have been discovered
to influence ageing in the nematode.
In the last part, I will present
some of our own work
that directly implicates
mitochondrial turnover
in the regulation
of organism lifespan,
and which demonstrates
the versatility of C. elegans
as a tool to dissect
the cellular and molecular
underpinnings of ageing.
1:04
Senescent decline in ageing
is driven by the inexorable
and random incidents of damage
to cellular constituents.
This continued white noise
of random molecular damage
forms the bedrock
for the advent of ageing.
In turn, molecular damage leads
to accumulation of cellular defects
that gradually and in time
precipitate a decline
in the function of cells,
organs, and tissues,
which can be manifested
as age-related frailty,
disability and disease.
1:37
The source of damage can be
both intrinsic and extrinsic.
Damaging agents can target
a variety of
important micromolecules,
such as DNA, proteins and lipids,
but also essential organs
in the cells, such as mitochondria.
Examples of agents and causes of
damage originating within the cell
are the byproducts
of metabolic processes,
such as oxidizing
reactive oxygen species,
as well as errors during
molecular synthesis processes.
Outside damaging factors
include UV radiation,
chemicals, toxins,
and heat among others.
Both intrinsic
and extrinsic factors
conspire to bring about ageing
and senescent decline.
Numerous diverse organisms
ranging from microbes to primates
have been used towards
understanding
the cellular
and molecular basis of ageing.
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