Chromosomes are pulled apart during mitosis; this not a gentle process. To prevent this important genetic information from being lost from the ends of the chromosome, telomeres protect this important information from being lost by taking the loss of its own base pairs. During mitosis, when the telomeres lose some base pairs, they can remain shortened and lead to further breakdown of the telomere, or the enzyme telomerase can add new base pairs allowing new generations of daughter cells to follow. A wild-type (WT) yeast mother cell will stop going through mitosis when it has created about 25 daughter cells. When the telomerase is inactivated, shortening occurs in the late after telomerase inactivation (LTI) which has similarities to normal …show more content…
showed that the LTI senescence was different from the ETI mother cell aging. In their work, Xie, et al. was also able to eliminate various causes of accelerated aging and found that the length of the telomere was not the cause of the rapid aging during ETI.
To perform their experiments, cells were created that had deleted, mutated, or a combination of both to test their hypotheses. An important cell population, tlc1∆, had its RNA template for telomerase deleted; therefore independently, or in combination with other mutations, these cells would not be able to activate telomerase. Combinations with sml1 ∆, tel1 ∆, and mrc1AQ were used in these experiments because each has a specific function that will be discussed further.
An important part of this paper was to compare the ETI and LTI terminal morphologies. There are three forms of terminal morphologies that can occur and with it, different mitochondrial localized GFP (mtGFP). With aging, the WT mother cell is seen as small buds and no fluorescence is seen. The second form has an elongated shape and fluorescence is visible within the cell. In the third form, the cell is shaped like a dumbbell and there are bright dots that can be seen within the