Normally these vital end caps protect the loose
ends of chromosomes from being chewed up or joined together, but are themselves whittled down every time the cell divides.
Telomeres are repetitive sequences of DNA that protect
the ends of chromosomes from deteriorating.
These mutations deactivate the POT1 gene that protects
the ends of our chromosomes from damage.
These DNA repeats are part of the protective capping structures, termed «telomeres,» which safeguard
the ends of chromosomes from unwanted and unwarranted DNA rearrangements that destabilize the genome.
Telomeres are bits of DNA that protect
the ends of chromosomes from unraveling or degrading.
Telomeres, compound structures at the end of each chromosome that protects
the end of the chromosome from deterioration, are the genetic key to longevity.
Telomeres are repetitive DNA sequences that protect
the end of the chromosome from being recognized as sites of DNA damage.
Not exact matches
Doing so keeps the telomeres found on the
ends of your DNA strands long and able to protect
chromosomes from deterioration.
«The whole process took about eight days,» Marks explains «and the inactivation spreads out
from the centre
of the X
chromosome towards the
ends.
Telomeres are repetitive stretches
of DNA that cap natural
chromosome ends to protect them
from being damaged or fused together during DNA replication.
Telomere proteins
from ciliated protozoa bind to the single - stranded G - rich DNA extensions at the
ends of macronuclear
chromosomes.
The researchers suspected that early damage
from exonucleases might be going unnoticed because the uncapped
ends of chromosomes fuse soon afterward.
Individuals carrying the variant had shorter telomeres, stretches
of DNA at the
ends of chromosomes that protect them
from daily wear — and also aging
Scientists long suspected they stabilized the structure
of the
chromosome, preventing the tips
from fraying, much like the plastic sheaths at the
ends of shoelaces to prevent them
from unraveling.
Telomeres are the caps at the
end of chromosomes that keep them
from shrinking when cells replicate.
The protein produced by this gene protects the
chromosome ends of the DNA
from damage, and controls telomere maintenance by the telomerase enzyme.
Biological age, Samani says, is related to the length
of telomeres — stretches
of DNA at the
ends of chromosomes, which protect these precious packages
of genes
from daily wear and tear.
Research
from the laboratory
of Chen and his colleagues, Yinnan Chen, Joshua Podlevsky and Dhenugen Logeswaran, recently uncovered a crucial step in the telomerase catalytic cycle that limits the ability
of telomerase to synthesize telomeric DNA repeats onto
chromosome ends.
A molecular biologist born in Hobart, Australia, Blackburn is best known for her 2009 Nobel Prize — winning discovery
of telomeres, caps on the
ends of chromosomes that protect genetic information
from damage and are thought to play an important role in aging and cancer.
They found that the inactivation
of POT1 caused by these mutations leads to longer and potentially unprotected telomeres, regions at the
end of our
chromosomes that protect
chromosomes from damage.
Inflammation also erodes telomeres, the «caps» at the
ends of chromosomes that protect genes
from degradation, which can lead to early cell death, premature aging and even cancer.
Research
from other scientists at Johns Hopkins, he says, had suggested that some tumors, particularly those that affect the nervous system, have mutations in the ATRX gene, which produces proteins that appear to maintain the length
of telomeres, repetitive segments
of DNA on the
ends of chromosomes that typically shorten each time a cell divides.
Telomeres are repetitive nucleotide sequences found at the
end of chromosomes which protect them
from deteriorating during the process
of replication.
Scientists at King's College London have found that people who have previously suffered
from acne are likely to have longer telomeres (the protective repeated nucleotides found at the
end of chromosomes) in their white blood cells, meaning their cells could be better protected against aging.
Dang's team traced the clumping back to malfunctions in the enzyme telomerase, which maintains the caps at the
ends of the
chromosomes and keeps the
chromosomes apart
from one another.
Telomeres are important because they stop
chromosomes from «fraying» or clumping together and «scrambling» the genetic codes they contain, performing a role similar to the plastic tips on the
end of shoelaces, to which they have been likened.
In this situation, the movement
of broken
ends can cause pieces
from different
chromosomes to stick together, forming monster
chromosomes that kill the cell.
Researchers at The Ohio State University examined blood
from pregnant women to evaluate the length
of telomeres — structures at the
end of chromosomes that are used by scientists as a measure
of biological (as opposed to chronological) age.
It helps to lengthen the telomeres — the proteins and DNA on the
ends of chromosomes that prevent dividing
chromosomes from fraying — and therefore increases the number
of times a cell can divide.
Because a trisomic cell contains two copies
of a
chromosome from one parent and one copy
of that
chromosome from the other parent, one in three embryos which revert
from trisomy to disomy will
end up with a pair
of chromosomes from just one parent.
Telomeres — repeating segments
of DNA on the
ends of chromosomes — are often likened to the plastic caps that prevent shoelaces
from fraying.
Researchers
from Leibniz Institute for Age Research — Fritz Lipmann Institute (Jena, Germany) now identified a crucial role
of telomeres, the
end structures
of chromosomes, for sensing cells with a wrong
chromosome number, referred to as aneuploidy.
Notably, the CRG team, which counted with the expertise in Mycoplasma
from the Serrano's laboratory and the collaboration
of the ICREA research professor Marc Marti - Renom at CNAG - CRG, discovered that Mycoplasma's circular
chromosome is consistently organised the same way in all the cells, with a region called the Origin (where DNA copying begins) at one
end of the structure and the midpoint
of the
chromosome located at the opposite
end.
The study, publishing online January 18 in the American Journal
of Epidemiology, found elderly women with less than 40 minutes
of moderate - to - vigorous physical activity per day and who remain sedentary for more than 10 hours per day have shorter telomeres — tiny caps found on the
ends of DNA strands, like the plastic tips
of shoelaces, that protect
chromosomes from deterioration and progressively shorten with age.
Telomeres (in white) cap the
ends of human
chromosomes, protecting the genetic information
from damage.
There are two known cases
of developmentally programmed locus - specific re-replication: Drosophila follicle cells, and salivary gland polytene
chromosomes from the
end of Sciara larval life.
Our lab studies various aspects
of chromosome biology ranging
from the maintenance
of chromosome ends by telomerase to meiosis, hybridization and ploidy.
Structures at the
end of chromosomes called telomeres protect cells
from deterioration or fusion with other
chromosomes.
Excess cortisol has been found to shorten the telomeres — the «caps» at the
ends of chromosomes that prevent them
from tangling with each other.
They protect
chromosome ends from being mistaken for broken pieces
of DNA that would otherwise be fixed by cellular repair machinery.
At the tips
of each
chromosome, at the
end of each DNA strand, there's a cap, like the tip
of a shoelace, which keeps our DNA
from unraveling and fraying.
New research
from a team at Karolinska University suggests that people who stand a lot have longer telomeres - caps on the
end of chromosomes which protect DNA
from wear and tear.