Covers how cells age at the chromosome level, starting with why linear eukaryotic chromosome ends shorten during replication because of lagging-strand primers. It then explains telomeres, their human TTAGGG repeat sequence and protective role, and telomerase as the enzyme that restores telomere length in germ cells and some stem cells. The note closes with free radical damage, oxidised proteins, and proteasomes that tag and degrade damaged proteins via ubiquitin.
Topic 16 of 63 in the MU Pleven syllabus for Biology (Medicine, Year 1). The free AceMed note covers it in 5 sections, about 428 words (3 min of reading), with 20 flashcards.
In this note
Aging and degradation of proteins.
Aging of Cells
Telomeres
Telomerase
Degradation of Proteins – Proteasomes
Aging of Cells
The Role of Telomeres
Unlike prokaryotic chromosomes, eukaryotic chromosomes are linear, meaning they have ends.
These ends cause problems during DNA replication because the DNA at the very end cannot be fully copied each round → gradual chromosome shortening.
At a replication fork:
Leading strand = continuous synthesis.
Lagging strand = made from Okazaki fragments, each beginning with an RNA primer.
Usually primers can be replaced with DNA, but at the chromosome end, there’s no space to place the final primer → part of the DNA is left un-copied.
The primer of the last Okazaki fragment also cannot be replaced, leaving a single-stranded overhang.
Over many cell divisions, this incomplete replication causes chromosomes to shorten progressively.
In humans, the last RNA primer can sit 70–100 nucleotides from the end → a long overhang and significant shortening each division.
Telomeres
To prevent gene loss, chromosome ends have telomeres, special DNA caps made of thousands of repeats.
In humans the sequence is: 5’-TTAGGG-3’.
Because telomeres have exposed single-stranded overhangs, they can look like damaged DNA, so they must be protected from repair systems.
The lagging-strand overhang comes from incomplete replication; the leading-strand overhang comes from enzymes cutting back the DNA.
In humans, telomeres can fold into protective loops with the help of proteins.
Telomere shortening is associated with cell aging: once telomeres reach a critical length, apoptosis is triggered.
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