• Title/Summary/Keyword: single nucleotide mismatch

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THE EFFECT OF GENETIC VARIATION IN THE DNA BASE REPAIR GENES ON THE RISK OF HEAD AND NECK CANCER (DNA 염기손상 치유유전자의 변이와 두경부암 발생 위험성)

  • Oh, Jung-Hwan;Yoon, Byung-Wook;Choi, Byung-Jun
    • Journal of the Korean Association of Oral and Maxillofacial Surgeons
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    • v.34 no.5
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    • pp.509-517
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    • 2008
  • DNA damage accumulates in cells as a result of exposure to exogenous agents such as benzopyrene, cigarette smoke, ultraviolet light, X-ray, and endogenous chemicals including reactive oxygen species produced from normal metabolic byproducts. DNA damage can also occur during aberrant DNA processing reactions such as DNA replication, recombination, and repair. The major of DNA damage affects the primary structure of the double helix; that is, the bases are chemically modified. These modification can disrupt the molecules'regular helical structure by introducing non-native chemical bonds or bulky adducts that do not fit in the standard double helix. DNA repair genes and proteins scan the global genome to detect and remove DNA damage and damage to single nucleotides. Direct reversal of DNA damage, base excision repair, double strand break. DNA repair are known relevant DNA repair mechanisms. Four different mechanisms are distinguished within excision repair: direct reversal, base excision repair, nucleotide excision repair, and mismatch repair. Genetic variation in DNA repair genes can modulate DNA repair capacity and alter cancer risk. The instability of a cell to properly regulate its proliferation in the presence of DNA damage increase risk of gene mutation and carcinogenesis. This article aimed to review mechanism of excision repair and to understand the relationship between genetic variation of excision repair genes and head and neck cancer.

A Gene-based dCAPS Marker for Selecting old-gold-crimson (ogc) Fruit Color Mutation in Tomato (토마토 과색 돌연변이 유전자(old-gold-crimson) 선발을 위한 dCAPS 분자표지 개발)

  • Park, Young-Hoon;Lee, Yong-Jae;Kang, Jum-Soon;Choi, Young-Whan;Son, Beung-Gu
    • Journal of Life Science
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    • v.19 no.1
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    • pp.152-155
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    • 2009
  • The old-gold-crimson ($og^c$) fruit color mutation produces deep red tomato fruit with high lycopene content. age is a null mutation allele of lycopene-${\beta}$-cyclase (Crt-b) gene (B locus) that converts lycopene to ${\beta}$-carotene in the cartenoid biosynthesis pathway in tomato. Breeding of high lycopene tomato cultivars can be accelerated by marker-assisted selection (MAS) for introgression of $og^c$ allele by using a gene-based DNA marker. In order to develop a marker, single nucleotide deletion of adenine(A) with. in a poly-A repeat that has been known to be responsible for frame-shift mutation of $og^c$ was confirmed by resequencing mutant allele and wild-type allele at B locus of several tomato lines. For allele discrimination and detection of $og^c$, derived CAPS (dCAPS) approach was used by designing a primer that artificially introduced restriction enzyme recognition site of Hin fI in PCR products from $og^c$ allele. This dCAPS marker is co-dominant gene-based PCR marker that can be efficiently used for MAS breeding program aiming the development of high lycopene tomato.