Molecular Mechanisms of DNA Damage and Repair: Progress in Plants

Abstract

Despite stable genomes of all living organisms, they are subject to damage by chemical and physical agents in the environment (e.g., UV and ionizing. radiations, chemical mutagens, fungal and bacterial toxins, etc.) and by free radicals or alkylating agents endogenously generated in metabolism. DNA is also damaged because of errors during its replication. The DNA lesions produced by these damaging agents could be altered base, missing base, mismatch base, deletion or insertion, linked pyrimidines, strand breaks, intra- and inter-strand cross-links. These DNA lesions could be genotoxic or cytotoxic to the cell. Plants are most affected by the UV-B radiation of sunlight, which penetrates and damages their genome by inducing oxidative damage (pyrimidine hydrates) and cross-links (both DNA protein and DNA-DNA) that are responsible for retarding the growth and development. The DNA lesions can be removed by repair, replaced by recombination, or retained, leading to genome instability or mutations or carcinogenesis or cell death. Mostly organisms respond to genome damage by activating a DNA damage response pathway that regulates cell-cycle arrest, apoptosis, and DNA repair pathways. To prevent the harmful effect of DNA damage and maintain the genome integrity, all organisms have developed various strategies to either reverse, excise, or tolerate the persistence of DNA damage products by generating a network of DNA repair mechanisms. A variety of different DNA repair pathways have been reported that include direct reversal, base excision repair, nucleotide excision repair, photoreactivation, bypass, double-strand break repair pathway, and mismatch repair pathway. The direct reversal and photoreactivation require single protein, all the rest of the repair mechanisms utilize multiple proteins to remove or repair the lesions. The base excision repair pathway eliminates single damaged base, while nucleotide excision repair excises a patch of 25- to 32-nucleotide-long oligomer, including the damage. The double-strand break repair utilizes either homologous recombination or nonhomologous endjoining. In plant the latter pathway is more error prone than in other eukaryotes, which could be an important driving force in plant genome evolution. The Arabidopsis genome data indicated that the DNA repair is highly conserved between plants and mammals than within the animal kingdom, perhaps reflecting common factors such as DNA methylation. This review describes all the possible mechanisms of DNA damage and repair in general and an up to date progress in plants. In addition, various types of DNA damage products, free radical production, lipid peroxidation, role of ozone, dessication damage of plant seed, DNA integrity in pollen, and the role of DNA helicases in damage and repair and the repair genes in Arabidopsis genome are also covered in this review.

Replication Protein A (RPA1a) Is Required for Meiotic and Somatic DNA Repair But Is Dispensable for DNA Replication and Homologous Recombination in Rice

“…MMC induces interstrand DNA cross-links that can be removed by HR, NER, and translesion synthesis pathways in eukaryotes (Lehoczky et al, 2007). UV irradiation induces DNA lesions such as cyclobutane pyrimidine dimers and pyrimidine (6-4) pyrimidinone dimers (6-4 photoproducts) that can be removed by photoreactivation and NER, BER, mismatch repair, and other DNA repair pathways (Tuteja et al, 2001;Kimura et al, 2004). In Arabidopsis, most of the genes involved in the control of meiotic chromosome dynamics are also required for DNA damage repair in somatic cells (Garcia et al, 2003;Waterworth et al, 2007), but their response spectrums are quite different.…”

Identification of Tyrosyl-DNA Phosphodiesterase as a Novel DNA Damage Repair Enzyme in Arabidopsis

“…Once DNA damage has occurred, specific DNA repair proteins, such as AP endonuclease, RAD1 (for radiation sensitive), RAD9, RAD51, XRCC2 (for x-ray repair crosscomplementing), Ku80 (XRCC6), and ligase, initiate to act through the repair pathways (Wood et al, 2001). Defects in DNA damage repair have evolved into cancer or genetic diseases in mammals and affect productivity or growth in plants (Tuteja et al, 2001;Wood et al, 2001). …”

Pengaruh Iradiasi Ultraviolet terhadap Multiplikasi Tunas Aksiler dan Kadar Klorofil Anyelir (Dianthus caryophyllus L.)

“…Fotoliase mengikat langsung ke dimer pirimidin, sehingga membentuk kompleks yang stabil dan dapat melakukan penyerapan foton untuk panjang gelombang yang sesuai (350-500 nm). Transfer foton diserap dari kromofor dari lyase ke dimer yang menginduksi pembalikan, kemudian memecah dimer dan menghasilkan dua monomer pirimidin (Tuteja et al, 2001). Pada tumbuhan, bahwa sebagian CPDs dan 6-4 fotoproduk dikeluarkan dari DNA oleh fotoreversal ditunjukkan oleh pengamatan bahwa sebagian fotoproduk hanya diperbaiki dalam kondisi cahaya (Britt, 1996).…”