The regulation of DNA repair during development

Abstract

DNA repair is important in such phenomena as carcinogenesis and aging. While much is known about DNA repair in single-cell systems such as bacteria, yeast, and cultured mammalian cells, it is necessary to examine DNA repair in a developmental context in order to completely understand its processes in complex metazoa such as man. We present data to support the notion that proliferating cells from organ systems, tumors, and embryos have a greater DNA repair capacity than terminally differentiated, nonproliferating cells. Differential expression of repair genes and accessibility of chromatin to repair enzymes are considered as determinants in the developmental regulation of DNA repair.

DNA photorepair in echinoid embryos: effects of temperature on repair rate in Antarctic and non-Antarctic species

“…Similarly, rotifer juveniles showed photoreactivation activity whereas adults showed no evidence of photoreactivation following UV-R exposure (Grad et al, 2003). It appears that photoreactivation rate is more efficient in developing embryos than in differentiated cells (Mitchell and Hartman, 1990), which would be consistent with our observations of greater repair in the earlier less differentiated embryonic stages.…”

“…Marine organisms can prevent this damage by passive methods with relatively low energetic costs such as sunscreens and non-enzymatic anti-oxidants (Dunlap et al, 2000), or by active, energetically costly, mechanisms such as antioxidant enzymes, photoreactivation and dark-excision DNA repair (Kim and Sancar, 1993;Malloy et al, 1997;Mitchell and Hartman, 1990). Three important points relevant to Antarctic embryos with very slow metabolism are: (i) the metabolic costs of active UV-R mitigation could result in reduced rates of repair; (ii) the continuously cold Antarctic waters would result in reduced activity of enzymes involved in UV-R mitigation if no cold-adaptation has occurred (Somero, 1995;Marshall, 1997) and; (iii) the low UV-R environment in the past may not have imposed selective pressures to evolve efficient UV-R mitigation strategies.…”

Variation in sunscreen compounds (mycosporine‐like amino acids) for marine species along a gradient of ultraviolet radiation transmission within doubtful sound, New Zealand

“…Marine organisms counteract the effects of ultraviolet radiation (UV-R) through a number of behavioural and physiological strategies, including negative-phototaxis (Pennington & Emlet 1986;Adams 2003), sunscreens , non-enzymatic antioxidants (Dunlap et al 2000), antioxidant enzymes (Lesser & Farrell 2004), DNA repair (Mitchell & Hartman 1990;Kim & Sancar 1993;Malloy et al 1997), and expression of cellcycle genes (Lesser et al 2001. Despite these mitigating strategies, UV-R can have detrimental influences on the marine environment at all trophic levels (see review by de Mora et al 2000).…”

An enzyme similar to animal type II photolyases mediates photoreactivation in Arabidopsis.

“…The role of photoreactivation in DNA repair in mammalian systems has been a subject of some debate (Sutherland and Sutherland, 1975;Harm, 1980;Friedberg, 1985;Li et al, 1993), although there is evidence that it does indeed occur (Sutherland and Bennett, 1995). It may be under developmental regulation (Mitchell and Hartman, 1990) because the process is pointless in internal tissues that receive neither UV nor photoreactivating light. In plants, there is physiological evidence for photoreactivation in the green alga Chlamydomonas (Rosen et al, 1980) and higher plants, including tobacco, bean, alfalfa, cucumber, and mustard (Trosko and Mansour, 1968;Beggs et al, 1985;Langer and Wellman, 1990;Takayanagi et al, 1994;Bucholz et al, 1995).…”