@article{rogers_bian_krakowsky_peters_turnbull_nelson_holland_2022, title={Genomic prediction for the Germplasm Enhancement of Maize project}, volume={10}, ISSN={["1940-3372"]}, url={https://doi.org/10.1002/tpg2.20267}, DOI={10.1002/tpg2.20267}, abstractNote={The Germplasm Enhancement of Maize (GEM) project was initiated in 1993 as a cooperative effort of public- and private-sector maize (Zea mays L.) breeders to enhance the genetic diversity of the U.S. maize crop. The GEM project selects progeny lines with high topcross yield potential from crosses between elite temperate lines and exotic parents. The GEM project has released hundreds of useful breeding lines based on phenotypic selection within selfing generations and multienvironment yield evaluations of GEM line topcrosses to elite adapted testers. Developing genomic selection (GS) models for the GEM project may contribute to increases in the rate of genetic gain. Here we evaluated the prediction ability of GS models trained on 6 yr of topcross evaluations from the two GEM programs in Raleigh, NC, and Ames, IA, documenting prediction abilities ranging from 0.36 to 0.75 for grain yield and from 0.78 to 0.96 for grain moisture when models were cross-validated within program and heterotic group. Predicted genetic gain from GS ranged from 0.95 to 2.58 times the gain from phenotypic selection. Prediction ability across program and heterotic group was generally poorer than within groups. Based on observed genomic relationships between GEM breeding lines and their tropical ancestors, GS for either yield or moisture would reduce recovery of exotic germplasm only slightly. Using GS models trained within program, the GEM programs should be able to more effectively deliver on its mission to broaden the genetic base of U.S. germplasm.}, journal={PLANT GENOME}, author={Rogers, Anna R. and Bian, Yang and Krakowsky, Matthew and Peters, David and Turnbull, Clint and Nelson, Paul and Holland, James B.}, year={2022}, month={Oct} }
 @article{lennon_krakowsky_goodman_flint-garcia_balint-kurti_2017, title={Identification of Teosinte Alleles for Resistance to Southern Leaf Blight in Near Isogenic Maize Lines}, volume={57}, ISSN={["1435-0653"]}, url={http://www.scopus.com/inward/record.url?eid=2-s2.0-85027562232&partnerID=MN8TOARS}, DOI={10.2135/cropsci2016.12.0979}, number={4}, journal={CROP SCIENCE}, author={Lennon, Jill R. and Krakowsky, Matthew and Goodman, Major and Flint-Garcia, Sherry and Balint-Kurti, Peter J.}, year={2017}, pages={1973–1983} }
 @article{lennon_krakowsky_goodman_flint-garcia_balint-kurti_2016, title={Identification of Alleles Conferring Resistance to Gray Leaf Spot in Maize Derived from its Wild Progenitor Species Teosinte}, volume={56}, ISSN={["1435-0653"]}, url={http://dx.doi.org/10.2135/cropsci2014.07.0468}, DOI={10.2135/cropsci2014.07.0468}, number={1}, journal={CROP SCIENCE}, author={Lennon, Jill R. and Krakowsky, Matthew and Goodman, Major and Flint-Garcia, Sherry and Balint-Kurti, Peter J.}, year={2016}, pages={209–218} }
 @article{jones_goodman_krakowsky_2016, title={Identification of maize-derived dominant gametophyte factors}, volume={209}, ISSN={["1573-5060"]}, DOI={10.1007/s10681-016-1635-0}, number={1}, journal={EUPHYTICA}, author={Jones, Zachary G. and Goodman, Major M. and Krakowsky, Matthew D.}, year={2016}, month={May}, pages={63–69} }
 @article{jones_goodman_krakowsky_2015, title={Identification of resistance to the Ga1-m gametophyte factor in maize}, volume={206}, ISSN={["1573-5060"]}, DOI={10.1007/s10681-015-1518-9}, number={3}, journal={EUPHYTICA}, author={Jones, Zachary G. and Goodman, Major M. and Krakowsky, Matthew D.}, year={2015}, month={Dec}, pages={785–791} }
 @misc{williams_krakowsky_scully_brown_menkir_warburton_windham_2015, title={Identifying and developing maize germplasm with resistance to accumulation of aflatoxins}, volume={8}, ISSN={["1875-0796"]}, DOI={10.3920/wmj2014.1751}, abstractNote={Efforts to identify maize germplasm with resistance to Aspergillus flavus infection and subsequent accumulation of aflatoxins were initiated by the US Department of Agriculture, Agricultural Research Service at several locations in the late 1970s and early 1980s. Research units at four locations in the south-eastern USA are currently engaged in identification and development of maize germplasm with resistance to A. flavus infection and accumulation of aflatoxins. The Corn Host Plant Resistance Research Unit, Mississippi State, MS, developed procedures for screening germplasm for resistance to A. flavus infection and accumulation of aflatoxins. Mp313E, released in 1990, was the first line released as a source of resistance to A. flavus infection. Subsequently, germplasm lines Mp420, Mp715, Mp717, Mp718, and Mp719 were released as additional sources of resistance. Quantitative trait loci associated with resistance have also been identified in four bi-parental populations. The Crop Protection and Management Research Unit and Crop Genetics and Breeding Research Unit, Tifton, GA, created a breeding population GT-MAS:gk. GT601, GT602, and GT603 were developed from GT-MAS:gk. The Food and Feed Safety Research Unit, New Orleans, LA, in collaboration with the International Institute for Tropical Agriculture used a kernel screening assay to screen germplasm and develop six germplasm lines with resistance to aflatoxins. The Plant Science Research Unit, Raleigh, NC, through the Germplasm Enhancement of Maize (GEM) Project provides to co-operators diverse germplasm that is a valuable source of resistance to A. flavus infection and accumulation of aflatoxins in maize.}, number={2}, journal={WORLD MYCOTOXIN JOURNAL}, author={Williams, W. P. and Krakowsky, M. D. and Scully, B. T. and Brown, R. L. and Menkir, A. and Warburton, M. L. and Windham, G. L.}, year={2015}, pages={193–209} }
 @article{belcher_zwonitzer_cruz_krakowsky_chung_nelson_arellano_balint-kurti_2012, title={Analysis of quantitative disease resistance to southern leaf blight and of multiple disease resistance in maize, using near-isogenic lines}, volume={124}, ISSN={["1432-2242"]}, url={http://www.scopus.com/inward/record.url?eid=2-s2.0-84860880839&partnerID=MN8TOARS}, DOI={10.1007/s00122-011-1718-1}, number={3}, journal={THEORETICAL AND APPLIED GENETICS}, publisher={Springer Science \mathplus Business Media}, author={Belcher, Araby R. and Zwonitzer, John C. and Cruz, Jose Santa and Krakowsky, Mathew D. and Chung, Chia-Lin and Nelson, Rebecca and Arellano, Consuelo and Balint-Kurti, Peter J.}, year={2012}, month={Feb}, pages={433–445} }
 @article{wisser_kolkman_patzoldt_holland_yu_krakowsky_nelson_balint-kurti_2011, title={Multivariate analysis of maize disease resistances suggests a pleiotropic genetic basis and implicates a GST gene}, volume={108}, ISSN={["0027-8424"]}, url={http://www.scopus.com/inward/record.url?eid=2-s2.0-79956318799&partnerID=MN8TOARS}, DOI={10.1073/pnas.1011739108}, abstractNote={Plants are attacked by pathogens representing diverse taxonomic groups, such that genes providing multiple disease resistance (MDR) are expected to be under positive selection pressure. To address the hypothesis that naturally occurring allelic variation conditions MDR, we extended the framework of structured association mapping to allow for the analysis of correlated complex traits and the identification of pleiotropic genes. The multivariate analytical approach used here is directly applicable to any species and set of traits exhibiting correlation. From our analysis of a diverse panel of maize inbred lines, we discovered high positive genetic correlations between resistances to three globally threatening fungal diseases. The maize panel studied exhibits rapidly decaying linkage disequilibrium that generally occurs within 1 or 2 kb, which is less than the average length of a maize gene. The positive correlations therefore suggested that functional allelic variation at specific genes for MDR exists in maize. Using a multivariate test statistic, a glutathione S -transferase ( GST ) gene was found to be associated with modest levels of resistance to all three diseases. Resequencing analysis pinpointed the association to a histidine (basic amino acid) for aspartic acid (acidic amino acid) substitution in the encoded protein domain that defines GST substrate specificity and biochemical activity. The known functions of GSTs suggested that variability in detoxification pathways underlie natural variation in maize MDR.}, number={18}, journal={PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA}, author={Wisser, Randall J. and Kolkman, Judith M. and Patzoldt, Megan E. and Holland, James B. and Yu, Jianming and Krakowsky, Matthew and Nelson, Rebecca J. and Balint-Kurti, Peter J.}, year={2011}, month={May}, pages={7339–7344} }
 @article{guo_krakowsky_ni_scully_lee_coy_widstrom_2011, title={Registration of Maize Inbred Line GT603}, volume={5}, ISSN={["1940-3496"]}, DOI={10.3198/jpr2010.08.0386crg}, abstractNote={ABSTRACTGT603 (Reg. No. GP-577, PI 659665) is an inbred line of yellow dent maize ( Zea mays L.) developed and released in 2010 by the USDA-ARS Crop Protection and Management Research Unit in cooperation with the University of Georgia Coastal Plain Experiment Station. GT603 was developed through seven generations of self-pollination from the maize population GT-MAS:gk (PI 561859), which was released as a source of resistance to Aspergillus fl avus Link:Fr. GT603 was initially selected from early self-pollinated lines under the experimental name GT-P50. Laboratory and fi eld studies demonstrated that GT603 had afl atoxin levels similar to or lower than the related inbred lines GT601 (PI 644026) and GT602 (PI 644027) and the controls Mp313E (PI539859) and Mp715 (PI614819), but it matured earlier than Mp313E and Mp715. The line GT603 is phenotypically different (darker cob and kernel colors and better agronomic traits) from the related lines GT601 and GT602 although the source of resistance may be the same. In hybrid performance tests in 2005 and 2009, GT603 exhibited better combining ability and heterosis with the Stiff Stalk Synthetic (SSS) inbred (B73) than with the non-SSS inbred (Mo17) for afl atoxin level and grain yield.}, number={2}, journal={JOURNAL OF PLANT REGISTRATIONS}, author={Guo, B. Z. and Krakowsky, M. D. and Ni, X. and Scully, B. T. and Lee, R. D. and Coy, A. E. and Widstrom, N. W.}, year={2011}, month={May}, pages={211–214} }
 @article{warburton_brooks_krakowsky_shan_windham_williams_2009, title={Identification and Mapping of New Sources of Resistance to Aflatoxin Accumulation in Maize}, volume={49}, ISSN={["1435-0653"]}, DOI={10.2135/cropsci2008.12.0696}, abstractNote={Maize (Zea mays L.) susceptibility to ear rot and afl atoxin accumulation by Aspergillus fl avus (Link:Fr) has caused signifi cant economic losses for farmers in the U.S. over the past 30 years. Afl atoxin outbreaks are generally associated with high temperatures and low moisture levels common to the southern U.S. To identify afl atoxin accumulation resistance quantitative trait loci (QTL) and linked markers for markerassisted breeding (MAB), a genetic mapping population of F 2:3 family genotypes, increased by sib-mating, was developed from Mp717, a maize inbred resistant to afl atoxin accumulation, and NC300, a southern-adapted inbred with low levels of resistance and desirable agronomic traits. Replicated trials of the mapping population were subjected to A. fl avus inoculation in Tifton, GA and Starkville, MS in 2004 and 2005. Quantitative trait loci on all chromosomes, except chromosomes 4, 6, and 9, were identifi ed, and individual QTL explained from less than 1% to a maximum of 11% of the phenotypic variance in afl atoxin accumulation in grain. Both Mp717 and NC300 were found to contribute resistance to afl atoxin accumulation in the F 2:3 families and overall QTL effects differed because of environmental conditions. Many of these loci were distinct from previously identifi ed QTL, which confi rmed Mp717 as a novel source of afl atoxin resistance.}, number={4}, journal={CROP SCIENCE}, author={Warburton, Marilyn L. and Brooks, Thomas. D. and Krakowsky, Matthew D. and Shan, Xueyan and Windham, Gary L. and Williams, W. Paul}, year={2009}, pages={1403–1408} }