Dissecting DNA Damage Responses in Arabidopsis: A High-Throughput Sequencing Approach Public

http://ir.library.oregonstate.edu/concern/honors_college_theses/b5644t464

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  • Cells are constantly bombarded with mutagens, both endogenous and exogenous in origin. Endogenous sources of mutation include reactive oxygen species formed during aerobic respiration, replication errors by DNA polymerase, and spontaneous deamination and depurination (Jackson 2009). Exogenous sources of mutation include UV and ionizing radiation, aflatoxins, and polycyclic aromatic hydrocarbons (i.e. compounds found in diesel exhaust and cigarette smoke). As a result, thousands of DNA lesions are created every day. Lesions can stall and impede DNA transcription and replication if they are not removed by DNA repair mechanisms or bypassed by replication. Phosphoinositide 3-kinase (PI3-K) related protein kinases (PIKKs) regulate the DNA damage response in cells (Cimprich 2008). Commonly referred to as the “sentries to the gate of genome stability,” ataxia-telangiectasia mutated (ATM) and ATM and RAD3-related (ATR) promote signaling, cell cycle arrest, and DNA repair in the face of DNA damage. Arabidopsis thaliana plants lacking ATR, when irradiated with UVB, incur elevated stem cell death in growing root tips (Furukawa 2010). Programmed cell death (PCD) is an important protective mechanism that restores tissue homeostasis in stem cell niches and prevents the accumulation of irreparably damaged cells in tissues, albeit with a delay in growth. Without ATR to stabilize damaged replication forks, double strand breaks (DSBs) occur where there is persistent ssDNA, and ATM or ATR (partially redundant in this signaling capacity) initiate repair or PCD if DSBs accumulate. In plants lacking both ATR and ATM, UV-B irradiation results in less stem cell death than in wild type plants. In attempts to cross atr[superscript -/-] plants with an EMS-mutagenized line, we discovered a root terminating phenotype which appears to be dependent on ATR and an unknown gene (ursu). We are using Illumina high-throughput genome sequencing and bioinformatic techniques to map the location of this additional gene.
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