A5000851229- DNA Repair Mechanisms
- CRISPR and Genetic Engineering
- Plant Genetic and Mutation Studies
- Carcinogens and Genotoxicity Assessment
- PARP inhibition in cancer therapy
- Microtubule and mitosis dynamics
- Allelopathy and phytotoxic interactions
- Chromosomal and Genetic Variations
- Genetic factors in colorectal cancer
- Cancer-related Molecular Pathways
- Advanced biosensing and bioanalysis techniques
- Coastal wetland ecosystem dynamics
- Plant Diversity and Evolution
- DNA and Nucleic Acid Chemistry
- Plant and animal studies
- Focus Groups and Qualitative Methods
- Genetics, Aging, and Longevity in Model Organisms
- Genomics and Chromatin Dynamics
- Social Media in Health Education
- Marine and coastal ecosystems
- Muscle Physiology and Disorders
- Microbial Community Ecology and Physiology
- Sirtuins and Resveratrol in Medicine
- Plant Parasitism and Resistance
- Biological Control of Invasive Species
Georgetown University Medical Center
2012-2024
Georgetown University
2012-2024
Memorial Sloan Kettering Cancer Center
2010-2017
Duquesne University
2015
University of Pittsburgh Medical Center
2015
University of North Carolina at Chapel Hill
2004-2009
University of South Carolina
2004-2009
Kettering University
2009
Repair of DNA double-strand breaks (DSBs) must be properly orchestrated in diverse chromatin regions to maintain genome stability. The choice between two main DSB repair pathways, nonhomologous end-joining (NHEJ) and homologous recombination (HR), is regulated by the cell cycle as well context. Pericentromeric heterochromatin forms a distinct nuclear domain that enriched for repetitive sequences pose significant challenges Heterochromatic DSBs display specialized temporal spatial dynamics...
Genomic integrity often is compromised in tumor cells, as illustrated by genetic alterations leading to loss of heterozygosity (LOH). One mechanism LOH mitotic crossover recombination between homologous chromosomes, potentially initiated a double-strand break (DSB). To examine associated with DSB-induced interhomolog recombination, we analyzed events using reporter mouse embryonic stem cells derived from F1 hybrid embryos. In this study, were able identify although they occur only rarely...
Double-strand breaks (DSBs) must be accurately and efficiently repaired to maintain genome integrity. Depending on the organism receiving break, genomic location of DSB, cell-cycle phase in which it occurs, a DSB can by homologous recombination (HR), nonhomologous end-joining (NHEJ), or single-strand annealing (SSA). Two novel repair assays were developed determine contributions these pathways finely resolve event structures Drosophila melanogaster. Rad51-dependent is preferred pathway...
Significance Here, we establish a role for small RNAs in promoting transgenerational fertility via an endogenous temperature-sensitive silencing process that is promoted by the RNAi spreading defective (RSD)-2 and RSD-6 proteins, which have been implicated RNA interference response to exogenous double-stranded triggers. This could be broadly relevant maintenance of heterochromatin plausibly regulation aging somatic cells as they proliferate.
Bloom syndrome is a rare disorder associated with cancer predisposition and genomic instability caused by loss of the RecQ helicase BLM. The Drosophila ortholog BLM (DmBlm) required for accurate repair DNA double-strand gaps homologous recombination. Repair products from DmBlm mutants have shorter synthesis tract lengths compared to wild type are frequently deletions flanking break site. To determine mechanisms responsible deletion formation in absence DmBlm, we characterized after excision...
Double-strand breaks (DSBs) are particularly deleterious DNA lesions for which cells have developed multiple mechanisms of repair. One major mechanism DSB repair in mammalian is homologous recombination (HR), whereby a donor sequence used as template For this reason, HR DSBs also being exploited gene modification possible therapeutic approaches. sensitive to divergence, such that the cell has ways suppress between diverged ("homeologous") sequences. In report, we examined several aspects...
Aging is characterized by genome instability, which contributes to cancer formation and cell lethality leading organismal decline. The high levels of DNA double-strand breaks (DSBs) observed in old cells premature aging syndromes are likely a primary source but the underlying cause their still unclear. DSBs might result from higher damage or repair defects emerging with advancing age, pathways organisms poorly understood. Here, we show that premeiotic germline young flies have distinct...
The ability of a cell to sense and respond DNA damage is essential for genome stability. An important aspect the response arrest cycle, presumably allow time repair. Ataxia telangiectasia mutated (ATM) ATR are such cell-cycle control, but some observations suggest that they also play direct role in Drosophila ortholog ATR, MEI-41, mediates damage-dependent G2-M checkpoint. We examined MEI-41 repair double-strand breaks (DSBs) induced by P-element excision. found mei-41 mutants defective...
// Michael P. Croglio 1,* , Jefferson M. Haake Colin Ryan 1 Victor S. Wang Jennifer Lapier Jamie Schlarbaum Yaron Dayani Emma Artuso 3 Cristina Prandi Hinanit Koltai 4 Keli Agama 5 Yves Pommier Yu Chen 6 Lucas Tricoli 2 Jeannine R. LaRocque Christopher Albanese 2,7 and Ronit I. Yarden 1,2 Department of Human Science, NHS, Georgetown University Medical Center, NW, Washington DC, USA The Lombardi Comprehensive Cancer Chemistry, Turin, Italy Institute Plant Sciences, ARO, Volcani Bet Dagan,...
Shifts in myosin heavy chain (MHC) expression within skeletal muscle can be induced by a host of stimuli including, but not limited to, physical activity, alterations neural aging, and diet or obesity. Here, we hypothesized that both age long-term (2 year) high fat/high sugar (HFS) would induce slow to fast MHC shift the plantaris, soleus, extensor digitorum longus (EDL) muscles from rhesus monkeys. Furthermore, tested whether supplementation with resveratrol, naturally occurring compound...
Accurate repair of DNA double-strand breaks (DSBs) is essential for the maintenance genome integrity, as failure to DSBs can result in cell death. The has evolved two main mechanisms DSB repair: non-homologous end-joining (NHEJ) and homology-directed (HDR), which includes single-strand annealing (SSA) homologous recombination (HR). While certain factors like age state chromatin are known influence pathway choice, roles developmental stage, tissue type, sex have yet be elucidated...
The general public's preferences for modes of communication (other than in-person communication) medical test results were investigated. We hypothesized that patients would prefer a variety methods to receive common tests (blood cholesterol and colonoscopy) compared with genetics results.This study was cross-sectional survey.A total 409 participants responded the survey. Among these participants, ≥50% reported they comfortable receiving blood or colonoscopy via 4 7 non-in-person...
Abstract DNA double-strand breaks (DSBs) must be accurately repaired to maintain genomic integrity. DSBs can by homologous recombination (HR), which uses an identical sequence as a template restore the genetic information lost at break. Suppression of between diverged sequences is essential repair without aberrant and potentially mutagenic non-identical sequences, such Alu repeats in human genome. The mismatch (MMR) machinery has been found suppress murine cells. To test if this phenomenon...
DNA double-strand breaks (DSBs) are a particularly deleterious class of damage that threatens genome integrity. DSBs repaired by three pathways: nonhomologous-end joining (NHEJ), homologous recombination (HR), and single-strand annealing (SSA). Drosophila melanogaster Blm (DmBlm) is the ortholog Saccharomyces cerevisiae SGS1 human BLM, has been shown to suppress crossovers in mitotic cells repair gaps via HR. To further elucidate role DmBlm simple DSB, particular mechanisms, we utilized...
DNA double-strand breaks (DSBs) are especially toxic lesions that, if left unrepaired, can lead to wide-ranging genomic instability. Of the pathways available repair DSBs, most accurate is homologous recombination (HR), where a sequence used as donor template restore genetic information at break site. While much of biochemical aspects HR have been characterized, how machinery locates and discriminates between potential templates throughout genome remains elusive. We use Drosophila...
Abstract The ability to respond DNA damage and incomplete replication ensures proper duplication stability of the genome. Two checkpoint kinases, ATM ATR, are required for responses. In Drosophila, ATR ortholog (MEI-41) is essential preventing entry into mitosis in presence damage. absence MEI-41, heterozygosity E(mus304) mutation causes rough eyes. We found that a DNApol-α180, which encodes catalytic subunit polymerase α. did not find any defects resulting from reducing Polα by itself....
Abstract RecQ helicases are a family of proteins involved in maintaining genome integrity with functions DNA repair, recombination, and replication. The human helicase consists five helicases: BLM, WRN, RECQL, RECQL4, RECQL5. Inherited mutations result Bloom Syndrome ( BLM mutation), Werner WRN Rothmund-Thomson RECQL4 other genetic diseases, including cancer. is evolutionarily conserved, as Drosophila melanogaster have three members: DmBlm, DmRecQL4, DmRecQL5 DmWRNexo, which contains...
DNA double-strand breaks (DSBs) are a particularly genotoxic type of damage that can result in chromosomal aberrations. Thus, proper repair DSBs is essential to maintaining genome integrity. be repaired by non-homologous end joining (NHEJ), where ends processed before through ligation. Alternatively, homology-directed repair, either homologous recombination (HR) or single-strand annealing (SSA). Both types initiated resection. In cultured human cells, the protein CtIP has been shown play...