For more info about the Genetics & Genomics Graduate Program, visit the program's homepage
Comments are off

UFGI Publications Round-Up Week 9/12/2016

Na2CO3-responsive mechanisms in halophyte Puccinellia tenuiflora roots revealed by physiological and proteomic analyses.

Author information: Zhao Q1,2, Suo J2, Chen S3, Jin Y2, Ma X2, Yin Z2, Zhang Y1, Wang T4, Luo J5, Jin W5, Zhang X4, Zhou Z1, Dai S1,2.

1Key Laboratory of Forest Plant Ecology, Ministry of Education, Northeast Forestry University, Harbin 150040, China.
2Alkali Soil Natural Environmental Science Center, Northeast Forestry University, Key Laboratory of Saline-alkali Vegetation Ecology Restoration in Oil Field, Ministry of Education, Harbin 150040, China.
3Department of Biology, Genetics Institute, Plant Molecular and Cellular Biology Program, Interdisciplinary Center for Biotechnology Research, University of Florida, Gainesville, FL 32610, USA.
4Institute of Botany, Chinese Academy of Sciences, Beijing 100093, China.
5AB Sciex Asia Pacific Application Support Center, Shanghai 200233, China.

Journal: Scientific Reports

Date of e-pub: September 2016

Abstract: Soil alkalization severely affects crop growth and agricultural productivity. Alkali salts impose ionic, osmotic, and high pH stresses on plants. The alkali tolerance molecular mechanism in roots from halophyte Puccinellia tenuiflora is still unclear. Here, the changes associated with Na2CO3 tolerance in P. tenuiflora roots were assessed using physiological and iTRAQ-based quantitative proteomic analyses. We set up the first protein dataset in P. tenuiflora roots containing 2,671 non-redundant proteins. Our results showed that Na2CO3 slightly inhibited root growth, caused ROS accumulation, cell membrane damage, and ion imbalance, as well as reduction of transport and protein synthesis/turnover. The Na2CO3-responsive patterns of 72 proteins highlighted specific signaling and metabolic pathways in roots. Ca(2+) signaling was activated to transmit alkali stress signals as inferred by the accumulation of calcium-binding proteins. Additionally, the activities of peroxidase and glutathione peroxidase, and the peroxiredoxin abundance were increased for ROS scavenging. Furthermore, ion toxicity was relieved through Na(+) influx restriction and compartmentalization, and osmotic homeostasis reestablishment due to glycine betaine accumulation. Importantly, two transcription factors were increased for regulating specific alkali-responsive gene expression. Carbohydrate metabolism-related enzymes were increased for providing energy and carbon skeletons for cellular metabolism. All these provide new insights into alkali-tolerant mechanisms in roots.

 

 

Setd1a and NURF mediate chromatin dynamics and gene regulation during erythroid lineage commitment and differentiation.

Author information: Li Y1, Schulz VP2, Deng C3, Li G4, Shen Y3, Tusi BK3, Ma G5, Stees J3, Qiu Y6, Steiner LA7, Zhou L8, Zhao K9, Bungert J10, Gallagher PG11, Huang S12.

1Department of Biochemistry and Molecular Biology, University of Florida College of Medicine, Gainesville, FL 32610, USA Macau Institute for Applied Research in Medicine and Health, State Key laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Avenida Wai Long, Taipa, Macau 519020, China.
2Department of Pediatrics, Pathology, and Genetics, Yale University School of Medicine, New Haven, CT 06520, USA.
3Department of Biochemistry and Molecular Biology, University of Florida College of Medicine, Gainesville, FL 32610, USA.
4Department of Molecular Genetics and Microbiology, University of Florida College of Medicine, Gainesville, FL 32610, USA.
5Public Health Studies, The Johns Hopkins University, Baltimore, MD 21218, USA.
6Department of Anatomy and Cell Biology, University of Florida College of Medicine, Gainesville, FL 32610, USA Genetics Institute, University of Florida, Gainesville, FL 32610, USA UF health Cancer center, University of Florida College of Medicine, Gainesville, FL 32610, USA.
7Department of Pediatrics, University of Rochester, Rochester, NY 14642, USA.
8Department of Molecular Genetics and Microbiology, University of Florida College of Medicine, Gainesville, FL 32610, USA Genetics Institute, University of Florida, Gainesville, FL 32610, USA UF health Cancer center, University of Florida College of Medicine, Gainesville, FL 32610, USA.
9Systems Biology Center, NHLBI, National Institute of Health, Bethesda, MD 20814, USA.
10Department of Biochemistry and Molecular Biology, University of Florida College of Medicine, Gainesville, FL 32610, USA Genetics Institute, University of Florida, Gainesville, FL 32610, USA.
11Department of Pediatrics, Pathology, and Genetics, Yale University School of Medicine, New Haven, CT 06520, USA Patrick.gallagher@yale.edu.
12Department of Biochemistry and Molecular Biology, University of Florida College of Medicine, Gainesville, FL 32610, USA Macau Institute for Applied Research in Medicine and Health, State Key laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Avenida Wai Long, Taipa, Macau 519020, China Genetics Institute, University of Florida, Gainesville, FL 32610, USA UF health Cancer center, University of Florida College of Medicine, Gainesville, FL 32610, USA sumingh@ufl.edu.

Journal: Nucleic Acids Research

Date of e-pub: September 2016

Abstract: The modulation of chromatin structure is a key step in transcription regulation in mammalian cells and eventually determines lineage commitment and differentiation. USF1/2, Setd1a and NURF complexes interact to regulate chromatin architecture in erythropoiesis, but the mechanistic basis for this regulation is hitherto unknown. Here we showed that Setd1a and NURF complexes bind to promoters to control chromatin structural alterations and gene activation in a cell context dependent manner. In human primary erythroid cells USF1/2, H3K4me3 and the NURF complex were significantly co-enriched at transcription start sites of erythroid genes, and their binding was associated with promoter/enhancer accessibility that resulted from nucleosome repositioning. Mice deficient for Setd1a, an H3K4 trimethylase, in the erythroid compartment exhibited reduced Ter119/CD71 positive erythroblasts, peripheral blood RBCs and hemoglobin levels. Loss of Setd1a led to a reduction of promoter-associated H3K4 methylation, inhibition of gene transcription and blockade of erythroid differentiation. This was associated with alterations in NURF complex occupancy at erythroid gene promoters and reduced chromatin accessibility. Setd1a deficiency caused decreased associations between enhancer and promoter looped interactions as well as reduced expression of erythroid genes such as the adult β-globin gene. These data indicate that Setd1a and NURF complexes are specifically targeted to and coordinately regulate erythroid promoter chromatin dynamics during erythroid lineage differentiation.

 

 

Functional Annotations of Paralogs: A Blessing and a Curse.

Author information: Zallot R1, Harrison KJ2, Kolaczkowski B3, de Crécy-Lagard V4.

1Department of Microbiology and Cell Science, Institute of Food and Agricultural Sciences, University of Florida, Gainesville, FL 32611, USA. remizallot@ufl.edu.
2Department of Microbiology and Cell Science, Institute of Food and Agricultural Sciences, University of Florida, Gainesville, FL 32611, USA. katherinejh@ufl.edu.
3Department of Microbiology and Cell Science, Institute of Food and Agricultural Sciences, University of Florida, Gainesville, FL 32611, USA. bryank@ufl.edu.
4Department of Microbiology and Cell Science, Institute of Food and Agricultural Sciences, University of Florida, Gainesville, FL 32611, USA. vcrecy@ufl.edu.

Journal: Life (Basel, Switzerland)

Date of e-pub: September 2016

Abstract: Gene duplication followed by mutation is a classic mechanism of neofunctionalization, producing gene families with functional diversity. In some cases, a single point mutation is sufficient to change the substrate specificity and/or the chemistry performed by an enzyme, making it difficult to accurately separate enzymes with identical functions from homologs with different functions. Because sequence similarity is often used as a basis for assigning functional annotations to genes, non-isofunctional gene families pose a great challenge for genome annotation pipelines. Here we describe how integrating evolutionary and functional information such as genome context, phylogeny, metabolic reconstruction and signature motifs may be required to correctly annotate multifunctional families. These integrative analyses can also lead to the discovery of novel gene functions, as hints from specific subgroups can guide the functional characterization of other members of the family. We demonstrate how careful manual curation processes using comparative genomics can disambiguate subgroups within large multifunctional families and discover their functions. We present the COG0720 protein family as a case study. We also discuss strategies to automate this process to improve the accuracy of genome functional annotation pipelines.

 

 

Immortalization of human normal and NF1 neurofibroma Schwann cells.

Author information: Li H1, Chang LJ1, Neubauer DR2, Muir DF2,3,4, Wallace MR1,4,5.

1Department of Molecular Genetics and Microbiology, University of Florida College of Medicine, Gainesville, FL, USA.
2Department of Pediatrics, Child Health Research Institute, University of Florida College of Medicine, Gainesville, FL, USA.
3Department of Neuroscience, University of Florida College of Medicine, Gainesville, FL, USA.
4University of Florida Health Cancer Center, University of Florida, Gainesville, FL, USA.
5University of Florida Genetics Institute, University of Florida, Gainesville, FL, USA.

Journal: Laboratory Investigation

Date of e-pub: September 2016

Abstract: Neurofibromas, which are benign Schwann cell tumors, are the hallmark feature in the autosomal dominant condition neurofibromatosis 1 (NF1) and are associated with biallelic loss of NF1 gene function. There is a need for effective therapies for neurofibromas, particularly the larger, plexiform neurofibromas. Tissue culture is an important tool for research. However, it is difficult to derive enriched human Schwann cell cultures, and most enter replicative senescence after 6-10 passages, impeding cell-based research in NF1. Through exogenous expression of human telomerase reverse transcriptase and murine cyclin-dependent kinase (mCdk4), normal (NF1 wild-type), neurofibroma-derived Schwann cells heterozygous for NF1 mutation, and neurofibroma-derived Schwann cells homozygous for NF1 mutation were immortalized, including some matched samples from the same NF1 patient. Initial experiments employed retroviral vectors, while subsequent work utilized lentiviral vectors carrying these genes because of improved efficiency. Expression of both transgenes was required for immortalization. Molecular and immunohistochemical analysis indicated that these cell lines are of Schwann cell lineage and have a range of phenotypes, many of which are consistent with their primary cultures. This is the first report of immortalization and detailed characterization of multiple human NF1 normal nerve and neurofibroma-derived Schwann cell lines, which will be highly useful research tools to study NF1 and other Schwann tumor biology and conditions.Laboratory Investigation aadvance online publication, 12 September 2016; doi:10.1038/labinvest.2016.88.

 

 

Ethical issues in the evaluation of adults with suspected genetic neuromuscular disorders.

Author information: Su X1, Kang PB2, Russell JA3, Simmons Z4.

1Department of Neurology, University of Pittsburgh Medical Center, Pittsburgh, PA, USA.
2Division of Pediatric Neurology, University of Florida College of Medicine, Gainesville, FL, USA.
3Section of Neurology, Lahey Hospital and Medical Center, Burlington, MA, USA.
4Departments of Neurology and Humanities, Penn State Hershey Medical Center, Hershey, PA, USA. zsimmons@hmc.psu.edu.

Journal: Muscle & Nerve

Date of e-pub: September 2016

Abstract: Genetic testing is rapidly becoming an increasingly significant part of the diagnostic armamentarium of neuromuscular clinicians. Although technically easy to order, the results of such testing, whether positive or negative, have potentially enormous consequences for the individual tested and for family members. As a result, ethical considerations must be in the forefront of the physician’s agenda when obtaining genetic testing. Informed consent is an important starting point for discussions between physicians and patients, but the counseling embedded in the informed consent process must be an ongoing part of subsequent interactions, including return of results and follow-up. Patient autonomy, including the right to know and right not-to-know results, must be respected. Considerations of capacity, physician beneficence and non-maleficence, and privacy all play roles in the process.

 

 

Role of host-driven mutagenesis in determining genome evolution of sigma virus (DMelSV; Rhabdoviridae) in Drosophila melanogaster.

Author information: Piontkivska H1, Matos LF2, Paul S3, Scharfenberg B4, Farmerie WG5, Miyamoto MM6, Wayne ML7.

1Department of Biological Sciences, Kent State University, Kent, OH 44242, USA opiontki@kent.edu.
2Department of Entomology & Nematology, University of Florida, Gainesville, FL 32611, USA Department of Biology, Eastern Washington University, Cheney, WA 99004, USA.
3Department of Biological Sciences, Kent State University, Kent, OH 44242, USA La Jolla Institute for Allergy and Immunology, La Jolla, CA, USA.
4Department of Biological Sciences, Kent State University, Kent, OH 44242, USA.
5Interdisciplinary Center for Biotechnology Research, University of Florida, Gainesville, FL 32611, USA.
6Department of Biology, University of Florida, Gainesville, FL 32611, USA.
7Department of Biology, University of Florida, Gainesville, FL 32611, USA Emerging Pathogens Institute, University of Florida, Gainesville, FL32611, USA.

Journal: Genome Biology and Evolution

Date of e-pub: September 2016

Abstract: Sigma virus (DMelSV) is ubiquitous in natural populations of Drosophila melanogaster Host-mediated, selective RNA editing of adenosines to inosines (ADAR) may contribute to control of viral infection by preventing transcripts from being transported into the cytoplasm or being translated accurately; or by increasing the viral genomic mutation rate. Previous PCR-based studies showed that ADAR mutations occur in DMelSV at low frequency. Here we use SOLiDTM deep sequencing of flies from a single host population from Athens, GA, USA to comprehensively evaluate patterns of sequence variation in DMelSV with respect to ADAR. GA dinucleotides, which are weak targets of ADAR, are strongly overrepresented in the positive strand of the virus, consistent with selection to generate ADAR resistance on this complement of the transient, double-stranded, RNA intermediate in replication and transcription. Potential ADAR sites in a worldwide sample of viruses are more likely to be “resistant” if the sites do not vary among samples. Either variable sites are less constrained and hence are subject to weaker selection than conserved sites, or the variation is driven by ADAR. We also find evidence of mutations segregating within hosts, hereafter referred to as hypervariable sites. Some of these sites were variable only in one or two flies (i.e. rare); others were shared by four or even all five of the flies (i.e. common). Rare and common hypervariable sites were indistinguishable with respect to susceptibility to ADAR; however, polymorphism in rare sites were more likely to be consistent with the action of ADAR than in common ones, again suggesting that ADAR is deleterious to the virus. Thus, in DMelSV, host mutagenesis is constraining viral evolution both within and between hosts.

 

 

Dietary Zinc Regulates Apoptosis through the p-elF2α/ATF4/CHOP Pathway during Pharmacologically Induced Endoplasmic Reticulum Stress in Livers of Mice.

Author information: Kim MH1, Aydemir TB1, Cousins RJ2.

1Food Science and Human Nutrition, and Center for Nutritional Sciences, College of Agricultural and Life Sciences, University of Florida,Gainesville, FL.
2Food Science and Human Nutrition, and Center for Nutritional Sciences, College of Agricultural and Life Sciences, University of Florida,Gainesville, FL cousins@ufl.edu.

Journal: The Journal of Nutrition

Date of e-pub: September 2016

Abstract: Several in vitro studies have shown that zinc deficiency could induce endoplasmic reticulum (ER) stress, resulting in activation of the unfolded protein response.

We aimed to determine whether consumption of a zinc-deficient diet (ZnD) triggers ER stress and to understand the impact of dietary zinc intake on ER stress-induced apoptosis using a mouse model.

Young adult (8-16 wk of age) male mice of strain C57BL/6 were fed either a ZnD (<1 mg/kg diet), or a zinc-adequate diet (ZnA; 30 mg/kg diet). After 2 wk, liver, pancreas, and serum samples were collected and analyzed for indexes of ER stress. In another experiment, mice were fed either a ZnD, a ZnA, or a zinc-supplementation diet (ZnS; 180 mg/kg diet). After 2 wk, vehicle or tunicamycin (TM; 2 mg/kg body weight) was administered to mice to model ER stress. Liver and serum were analyzed for indexes of ER stress to evaluate the effects of zinc status.

Mice fed a ZnD did not activate the apoptotic and ER stress markers in the liver or pancreas. During the TM challenge, mice fed a ZnD showed greater C/EBP-homologous protein expression in the liver (3.8-fold, P < 0.01) than did ZnA-fed mice. TM-treated mice fed a ZnD also had greater terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick-end labeling-positive cells in the liver (2.2-fold, P < 0.05), greater hepatic triglyceride accumulation (1.5-fold, P < 0.05), greater serum alanine aminotransferase activity (1.6-fold, P < 0.05), and greater protein-tyrosine phosphatase 1B activity (1.5-fold, P < 0.05), respectively, than did those fed a ZnA. No significant differences were observed in these parameters between mice fed ZnAs and ZnSs.

Consumption of a ZnD per se is not a critical factor for induction of ER stress in mice; however, once ER stress is triggered, adequate dietary zinc intake is required for suppressing apoptotic cell death and further insults in the liver of mice.

 

 

Clinical Effects of Driver Somatic Mutations on the Outcomes of Patients With Myelodysplastic Syndromes Treated With Allogeneic Hematopoietic Stem-Cell Transplantation.

Author information: Della Porta MG1, Gallì A2, Bacigalupo A2, Zibellini S2, Bernardi M2, Rizzo E2, Allione B2, van Lint MT2, Pioltelli P2, Marenco P2, Bosi A2, Voso MT2, Sica S2,Cuzzola M2, Angelucci E2, Rossi M2, Ubezio M2, Malovini A2, Limongelli I2, Ferretti VV2, Spinelli O2, Tresoldi C2, Pozzi S2, Luchetti S2, Pezzetti L2, Catricalà S2, Milanesi C2, Riva A2, Bruno B2, Ciceri F2, Bonifazi F2, Bellazzi R2, Papaemmanuil E2, Santoro A2, Alessandrino EP2, Rambaldi A2, Cazzola M2.

1Matteo G. Della Porta, Anna Gallì, Silvia Zibellini, Ettore Rizzo, Marianna Rossi, Marta Ubezio, Virginia V. Ferretti, Silvia Catricalà, Chiara Milanesi, Emilio P. Alessandrino, and Mario Cazzola, Fondazione IRCCS Policlinico, San Matteo; Matteo G. Della Porta, Alberto Malovini, Ivan Limongelli, Riccardo Bellazzi, and Mario Cazzola, University of Pavia, Pavia; Andrea Bacigalupo, Maria Teresa van Lint, Sarah Pozzi, and Silvia Luchetti, San Martino Hospital, Genova; Massimo Bernardi, Cristina Tresoldi, and Fabio Ciceri, San Raffaele Scientific Institute; Paola Marenco and Laura Pezzetti, Ospedale Niguarda Ca’ Granda, Milan; Bernardino Allione and Benedetto Bruno, University of Torino, Torino; Pietro Pioltelli, Ospedale San Gerardo, Monza; Alberto Bosi, Azienda Ospedaliera Universitaria Careggi, Florence; Maria Teresa Voso and Simona Sica, Catholic University of the Sacred Heart, Rome; Mariella Cuzzola, Azienda Ospedaliera Bianchi Melacrino Morelli, Reggio Calabria; Emanuele Angelucci, Ospedale Oncologico di Riferimento Regionale A. Businco, Cagliari; Orietta Spinelli and Alessandro Rambaldi, Azienda Ospedaliera Papa Giovanni XXIII, Bergamo; Francesca Bonifazi, University of Bologna, Bologna; Armando Santoro, Humanitas University, Rozzano, Italy; Alberto Riva, University of Florida, Gainesville, FL; and Elli Papaemmanuil, Memorial Sloan-Kettering Cancer Center, New York, NY. matteogiovanni.dellaporta@unipv.it.
2Matteo G. Della Porta, Anna Gallì, Silvia Zibellini, Ettore Rizzo, Marianna Rossi, Marta Ubezio, Virginia V. Ferretti, Silvia Catricalà, Chiara Milanesi, Emilio P. Alessandrino, and Mario Cazzola, Fondazione IRCCS Policlinico, San Matteo; Matteo G. Della Porta, Alberto Malovini, Ivan Limongelli, Riccardo Bellazzi, and Mario Cazzola, University of Pavia, Pavia; Andrea Bacigalupo, Maria Teresa van Lint, Sarah Pozzi, and Silvia Luchetti, San Martino Hospital, Genova; Massimo Bernardi, Cristina Tresoldi, and Fabio Ciceri, San Raffaele Scientific Institute; Paola Marenco and Laura Pezzetti, Ospedale Niguarda Ca’ Granda, Milan; Bernardino Allione and Benedetto Bruno, University of Torino, Torino; Pietro Pioltelli, Ospedale San Gerardo, Monza; Alberto Bosi, Azienda Ospedaliera Universitaria Careggi, Florence; Maria Teresa Voso and Simona Sica, Catholic University of the Sacred Heart, Rome; Mariella Cuzzola, Azienda Ospedaliera Bianchi Melacrino Morelli, Reggio Calabria; Emanuele Angelucci, Ospedale Oncologico di Riferimento Regionale A. Businco, Cagliari; Orietta Spinelli and Alessandro Rambaldi, Azienda Ospedaliera Papa Giovanni XXIII, Bergamo; Francesca Bonifazi, University of Bologna, Bologna; Armando Santoro, Humanitas University, Rozzano, Italy; Alberto Riva, University of Florida, Gainesville, FL; and Elli Papaemmanuil, Memorial Sloan-Kettering Cancer Center, New York, NY.

Journal: The Journal of Clinical Oncology

Date of e-pub: September 2016

Abstract: 

The genetic basis of myelodysplastic syndromes (MDS) is heterogeneous, and various combinations of somatic mutations are associated with different clinical phenotypes and outcomes. Whether the genetic basis of MDS influences the outcome of allogeneic hematopoietic stem-cell transplantation (HSCT) is unclear.

We studied 401 patients with MDS or acute myeloid leukemia (AML) evolving from MDS (MDS/AML). We used massively parallel sequencing to examine tumor samples collected before HSCT for somatic mutations in 34 recurrently mutated genes in myeloid neoplasms. We then analyzed the impact of mutations on the outcome of HSCT.

Overall, 87% of patients carried one or more oncogenic mutations. Somatic mutations of ASXL1, RUNX1, and TP53 were independent predictors of relapse and overall survival after HSCT in both patients with MDS and patients with MDS/AML (P values ranging from .003 to .035). In patients with MDS/AML, gene ontology (ie, secondary-type AML carrying mutations in genes of RNA splicing machinery, TP53-mutated AML, or de novo AML) was an independent predictor of posttransplantation outcome (P = .013). The impact of ASXL1, RUNX1, and TP53 mutations on posttransplantation survival was independent of the revised International Prognostic Scoring System (IPSS-R). Combining somatic mutations and IPSS-R risk improved the ability to stratify patients by capturing more prognostic information at an individual level. Accounting for various combinations of IPSS-R risk and somatic mutations, the 5-year probability of survival after HSCT ranged from 0% to 73%.

Somatic mutation in ASXL1, RUNX1, or TP53 is independently associated with unfavorable outcomes and shorter survival after allogeneic HSCT for patients with MDS and MDS/AML. Accounting for these genetic lesions may improve the prognostication precision in clinical practice and in designing clinical trials.

 

 

Identification of major QTLs underlying tomato spotted wilt virus resistance in peanut cultivar Florida-EP(TM) ‘113’.

Author information: Tseng YC1,2, Tillman BL3,4, Peng Z1, Wang J5,6.

1Agronomy Department, University of Florida, 2033 Mowry Road, Room 337 Cancer/Genetics Research Complex, Gainesville, FL, 32610, USA.
2North Florida Research and Education Center, University of Florida, Marianna, FL, 32446, USA.
3Agronomy Department, University of Florida, 2033 Mowry Road, Room 337 Cancer/Genetics Research Complex, Gainesville, FL, 32610, USA. btillman@ufl.edu.
4North Florida Research and Education Center, University of Florida, Marianna, FL, 32446, USA. btillman@ufl.edu.
5Agronomy Department, University of Florida, 2033 Mowry Road, Room 337 Cancer/Genetics Research Complex, Gainesville, FL, 32610, USA. wangjp@ufl.edu.
6Genetics Institute, Plant Molecular and Cellular Biology Program, University of Florida, Gainesville, FL, 32610, USA. wangjp@ufl.edu.

Journal: BMC Genetics

Date of e-pub: September 2016

Abstract: Spotted wilt caused by tomato spotted wilt virus (TSWV) is one of the major peanut (Arachis hypogaea L.) diseases in the southeastern United States. Occurrence, severity, and symptoms of spotted wilt disease are highly variable from season to season, making it difficult to efficiently evaluate breeding populations for resistance. Molecular markers linked to spotted wilt resistance could overcome this problem and allow selection of resistant lines regardless of environmental conditions. Florida-EP(TM) ‘113’ is a spotted wilt resistant cultivar with a significantly lower infection frequency. However, the genetic basis is still unknown. The objective of this study is to map the major quantitative trait loci (QTLs) linked to spotted wilt resistance in Florida-EP(TM) ‘113’.

Among 2,431 SSR markers located across the whole peanut genome screened between the two parental lines, 329 were polymorphic. Those polymorphic markers were used to further genotype a representative set of individuals in a segregating population. Only polymorphic markers on chromosome A01 showed co-segregation between genotype and phenotype. Genotyping by sequencing (GBS) of the representative set of individuals in the segregating population also depicted a strong association between several SNPs on chromosome A01 and the trait, indicating a major QTL on chromosome A01. Therefore marker density was enriched on the A01 chromosome. A linkage map with 23 makers on chromosome A01 was constructed, showing collinearity with the physical map. Combined with phenotypic data, a major QTL flanked by marker AHGS4584 and GM672 was identified on chromosome A01, with up to 22.7 % PVE and 9.0 LOD value.

A major QTL controlling the spotted wilt resistance in Florida-EP(TM) ‘113’ was identified. The resistance is most likely contributed by PI 576638, a hirsuta botanical-type line, introduced from Mexico with spotted wilt resistance. The flanking markers of this QTL can be used for further fine mapping and marker assisted selection in peanut breeding programs.

 

 

Integrating Domain Specific Knowledge and Network Analysis to Predict Drug Sensitivity of Cancer Cell Lines.

Author information: Kim S1, Sundaresan V2, Zhou L2, Kahveci T1.

1Department of Computer and Information Science and Engineering, University of Florida, Gainesville, FL, United States of America.
2Department of Molecular Genetics and Microbiology College of Medicine, University of Florida, Gainesville, FL, United States of America.

Journal: PLoS One

Date of e-pub: September 2016

Abstract: One of fundamental challenges in cancer studies is that varying molecular characteristics of different tumor types may lead to resistance to certain drugs. As a result, the same drug can lead to significantly different results in different types of cancer thus emphasizing the need for individualized medicine. Individual prediction of drug response has great potential to aid in improving the clinical outcome and reduce the financial costs associated with prescribing chemotherapy drugs to which the patient’s tumor might be resistant. In this paper we develop a network based classifier (NBC) method for predicting sensitivity of cell lines to anticancer drugs from transcriptome data. In the literature, this strategy has been used for predicting cancer types. Here, we extend it to estimate sensitivity of cells from different tumor types to various anticancer drugs. Furthermore, we incorporate domain specific knowledge such as the use of apoptotic gene list and clinical dose information in our method to impart biological significance to the prediction. Our experimental results suggest that our network based classifier (NBC) method outperforms existing classifiers in estimating sensitivity of cell lines for different drugs.

 

 

Genome-wide association study reveals putative regulators of bioenergy traits in Populus deltoides.

Author information: Fahrenkrog AM1,2, Neves LG1,2, Resende MF Jr1,3, Vazquez AI4, de Los Campos G4,5, Dervinis C1, Sykes R6, Davis M6, Davenport R7, Barbazuk WB2,7,8,Kirst M9,10,11.

1School of Forest Resources and Conservation, University of Florida, PO Box 110410, Gainesville, FL, 32611, USA.
2Plant Molecular and Cellular Biology Graduate Program, University of Florida, PO Box 110690, Gainesville, FL, 32610, USA.
3Genetics and Genomics Graduate Program, University of Florida, PO Box 103610, Gainesville, FL, 32610, USA.
4Department of Epidemiology and Biostatistics, Michigan State University, 909 Fee Road, East Lansing, MI, 48824, USA.
5Statistics Department, Michigan State University, 619 Red Cedar Road, MI, 48824, USA.
6National Renewable Energy Laboratory, 15013 Denver West Parkway, Golden, CO, 80401, USA.
7Biology Department, University of Florida, PO Box 118525, Gainesville, FL, 32611, USA.
8University of Florida Genetics Institute, University of Florida, PO Box 103610, Gainesville, FL, 32611, USA.
9School of Forest Resources and Conservation, University of Florida, PO Box 110410, Gainesville, FL, 32611, USA. mkirst@ufl.edu.
10Plant Molecular and Cellular Biology Graduate Program, University of Florida, PO Box 110690, Gainesville, FL, 32610, USA. mkirst@ufl.edu.
11University of Florida Genetics Institute, University of Florida, PO Box 103610, Gainesville, FL, 32611, USA. mkirst@ufl.edu.

Journal: New Phyltologist

Date of e-pub: September 2016

Abstract: Genome-wide association studies (GWAS) have been used extensively to dissect the genetic regulation of complex traits in plants. These studies have focused largely on the analysis of common genetic variants despite the abundance of rare polymorphisms in several species, and their potential role in trait variation. Here, we conducted the first GWAS in Populus deltoides, a genetically diverse keystone forest species in North America and an important short rotation woody crop for the bioenergy industry. We searched for associations between eight growth and wood composition traits, and common and low-frequency single-nucleotide polymorphisms detected by targeted resequencing of 18 153 genes in a population of 391 unrelated individuals. To increase power to detect associations with low-frequency variants, multiple-marker association tests were used in combination with single-marker association tests. Significant associations were discovered for all phenotypes and are indicative that low-frequency polymorphisms contribute to phenotypic variance of several bioenergy traits. Our results suggest that both common and low-frequency variants need to be considered for a comprehensive understanding of the genetic regulation of complex traits, particularly in species that carry large numbers of rare polymorphisms. These polymorphisms may be critical for the development of specialized plant feedstocks for bioenergy.

NOTE: These abstracts were retrieved from the U.S. National Library of Medicine website managed in collaboration with the U.S. National Library of Medicine 

About the Author