A balance between two genes
that help maintain normal cellular function has been found by
researchers at The Scripps Research Institute.
‘The interplay of Spns1 and Atp6v0ca genes may prevent Premature ageing, signaling the need for a healthy lifestyle.’
The two genes were
- Spns1- Induces degradation and
- atp6v0ca- Suppresses the degradation caused by Spns1 (Sphingolipid
Transporter 1 (putative))
The two genes work
together to suppress premature
ageing and increase lifespan, based on studies conducted on Zebra
fish. The results of the study were published in the Journal Autophagy
is associated with increase in wrinkles,
loss of fat, thinning of skin, loss of hair amongst others, however, in
premature aging, these symptoms could occur at a much earlier age. An individual
who shows signs of premature aging
could be at an increased risk
for disease found in older people and could also undergo emotional issues that
affect mental health.
Dr.Shuji Kishi who is the lead author of the study said "We found that the dual
defects did indeed counteract senescence during development and extended the
animal's survival and life span."
This study will aid in
highlighting the body's inability to dispose the build-up of harmful chemicals
and could fuel further research on ways to prevent such build ups.
Autophagy is a mechanism
by which cellular components are enveloped by the lysosome and degraded. This
process is believed to be a self-degradative process that aids in balancing
energy resources when there is energy stress in the body.
The protein encoded by
the gene spns1 is involved in autophagy in mammals like zebra fish and humans.
Autophagy helps to
- remove misfolded and aggregated
- Clear organelles that are damaged within the cell
- Eliminate intracellular
- Specifically or non-specifically remove organelles and protein
Defects in the spns1 (Sphingolipid
Transporter 1 (putative))gene were found to lead to senescence in the developing
embryos and premature ageing in adults. Dr. Kishi and his colleagues found that
defects in another gene called atp6v0ca counteracted the defect in the spns1
gene. The two genes are believed to balance the function that leads to normal
Between the Genes
There should be a
balance between the genes that will aid in preventing premature
aging. An insight into this balance will provide clues to lysosomal diseases
where the accumulation of waste products results in vacuoles in the lysosome.
The age of onset,
severity of the disease as well as the inclusion of the central nervous system
manifestation can vary within the disease. There are over 50 lysosomal diseases
which include Pompe disease, Tay Sach's, Gaucher and Salla. These lysosomal
diseases have infantile, juvenile and adult forms of disease.
The severity of the
disease depends on the type of waste stored in the lysosomes. In Pompe disease,
there is accumulation of glycogen in the lysosome which leads to muscle
The genes that have been
identified in the suppression of premature aging could be involved in the
synthesis of hormones which could aid in the removal of waste from the
lysozyme. Dr. Shanshan Lian who is a research associate and one of the first
author of the study said "The use of appropriate inhibitors, selective for
key steps in the biosynthesis of cellular macromolecules in general, may
restore normal dynamics in the autolysosomal compartment and correct the
pathological storage that is the ultimate cause of these types of disease."
The current study will
also aid in
- Identifying new genes which could
affect the aging process.
- High throughput
analysis of pharmacological factors which could accelerate aging
like oxygen radicals.
The process of autophagy
and apoptosis (programmed cell death) are required for cell renewal, older and
damaged tissues are destroyed using apoptosis and the energy is recycled. Stem
cells play an important role in replenishing the cells that undergo programmed
cell death. While the process of aging is normal, when this
process is advanced, resulting in symptoms that are normally identified in old
age but now being identified at an early stage, it is known as premature
There are many factors
that contribute to premature aging
- Metabolic Stress
An understanding of the
genes that play an important role in premature aging will aid in
tailoring lifestyle and diet to suit the specific needs of the patient. Interventional
therapies that maintain the balance between Spns1
1 (putative)) and atp6v0ca could be the next step in aging
. Individuals who show an imbalance could be provided with
protein therapy that compensate for the lack of protein synthesized by the
always been a condition that is wrought with worry about good physical and
mental health. There has been an increase in the number of years an individual
lives with the advent of technology but there has not been an increase in the
quality of life lead due to age related diseases. Studies such as these could
help in lowering the risk for disease and improving health during advanced
years of life.
- Autophagy: cellular and molecular
mechanisms - (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2990190/)
- Lysosomal Storage Disorders - (https://www.ncbi.nlm.nih.gov/books/NBK6177/)
- Aging: The Biology of Senescence -
- Cellular Mechanisms of Somatic Stem Cell
Aging - (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3982593/)