A Systematic Review of the Effects of the Two Major Types of Progeroid Syndromes (Hutchinson-Gilford and Werner) on the Factors of Aging Within DNA Replication.
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Olukemi Akintewe
Description
DNA replication, broadly defined, is the process by which a cell duplicates, occurring in three primary phases. Several errors occur within this process. Various stressors can damage the cell's genome during the S-phase, a by-product of the aging process. In progeroid syndromes, however, this process varies significantly. For example, in Hutchinson-Gilford Syndrome (HGS), a mutation in the LMNA gene, which produces Lamina-A, produces effects of accelerated aging resulting in the mislocation of a protein involved in the elongation step of DNA replication. Similarly, in Werner Syndrome (WS), a mutation in the Werner (WRN) gene produces protein nullification. It negatively impacts the progression of the DNA replication fork and subsequential recovery through double-strand break (DSB) repair. Both of these progeroid syndromes, while rare, produce accelerated signs of aging on the cellular level as well as a significantly reduced life expectancy. This paper seeks to show how mutations in proteins can cause the nullification of their function or aberrant functionality, leading to further damage of the genome in progeroid syndromes (aging disorders), including HGS and WS. The method of this systematic review was done using an online database search. N=556 articles; removed duplicates, N=23 were used for qualitative synthesis. Our findings suggest that mutations in the genes that code for replisomes can code for dysfunctional proteins, which could alter the replisomes' ability to replicate the genome successfully; this causes further genomic damage. Vitamin C and D/DVR were proven to help minimize adverse symptoms of accelerated aging in HGS and WS, respectively.
A Systematic Review of the Effects of the Two Major Types of Progeroid Syndromes (Hutchinson-Gilford and Werner) on the Factors of Aging Within DNA Replication.
DNA replication, broadly defined, is the process by which a cell duplicates, occurring in three primary phases. Several errors occur within this process. Various stressors can damage the cell's genome during the S-phase, a by-product of the aging process. In progeroid syndromes, however, this process varies significantly. For example, in Hutchinson-Gilford Syndrome (HGS), a mutation in the LMNA gene, which produces Lamina-A, produces effects of accelerated aging resulting in the mislocation of a protein involved in the elongation step of DNA replication. Similarly, in Werner Syndrome (WS), a mutation in the Werner (WRN) gene produces protein nullification. It negatively impacts the progression of the DNA replication fork and subsequential recovery through double-strand break (DSB) repair. Both of these progeroid syndromes, while rare, produce accelerated signs of aging on the cellular level as well as a significantly reduced life expectancy. This paper seeks to show how mutations in proteins can cause the nullification of their function or aberrant functionality, leading to further damage of the genome in progeroid syndromes (aging disorders), including HGS and WS. The method of this systematic review was done using an online database search. N=556 articles; removed duplicates, N=23 were used for qualitative synthesis. Our findings suggest that mutations in the genes that code for replisomes can code for dysfunctional proteins, which could alter the replisomes' ability to replicate the genome successfully; this causes further genomic damage. Vitamin C and D/DVR were proven to help minimize adverse symptoms of accelerated aging in HGS and WS, respectively.
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Poster Presentation