Critique Biological & Biomedical Sciences Article Critique

Article Critique
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Article Critique
The article provides new insights about telomeres, which are specialized structures that are heterochromatic and are located at the edges of the linear eukaryotic chromosomes, and they play an integral role in proliferation and cell survival. The somatic cells in humans undergo erosion arising from telomeric DNA each time they imprint their genome, and this is attribute to incapacity if the DNA polymerases to complete the gap that is left behind once the finally RNA primer is removed.
One strong attribute about the article is that it proves that once phosphorylation by threonine 271 in vivo, overexpression of TRF1 that ahs a failed mutation of monophosphorylate T271A will not result in telomere elongation. On the other hand, overexpression of TRF1, which has a phosphomimetic mutation of T271D, can limit the length of the telomere. The study also used HeLaII cell line as a control for stable expression of the two variables, pWZL, and pRetroSuper (pRS). For the analysis, the research relied on TRF1-depleted cells obtained from TRF1 to reduce the interference from endogenous TRF1.
Some of the misinterpretations from the article include the view that phosphomimetic mutation or nonphosphorylatable mutation of T271A can not impact TRF1 phosphorylation on the on T371 even though the information is unpublished. This could mean that it is not valid since the previous authors were not in support of the perspective.
Some of the minor problems with the data are that bioinformatics analysis does not provide a clear outcome of the kinase, which has a role in the phosphorylation site (RXXS/T) of Chk2 and Chk1. An improvement would be determining the Chk2 and Chk1 kinases that influence phosphorylating T271 in vivo. Studies will also have to focus on how T273 and T271 control the telomere synergistically to lengthen them.
Follow up experiments will have to focus ...