@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={AbstractThe 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={0011-183X 1435-0653}, url={http://dx.doi.org/10.2135/cropsci2016.12.0979}, DOI={10.2135/cropsci2016.12.0979}, abstractNote={Southern leaf blight ([SLB], causal agent Cochliobolus heterostrophus) is an important fungal disease of maize (Zea mays L.). Teosinte (Z. mays ssp. parviglumis), the wild progenitor of maize, offers a novel source of resistance alleles that may have been lost during domestication. The aims of this study were to identify teosinte alleles that, when present in a temperate maize background, confer a significant level of resistance to SLB. Ten populations of BC4S2 near isogenic lines (NILs), developed by crossing 10 different teosinte accessions to the maize inbred B73, comprising 774 lines in total, were screened for SLB resistance. Quantitative trait locus (QTL) analysis identified four significant QTL associated with SLB in bins 2.04, 3.04, 3.05, and 8.05. Sixteen individual NILs which were significantly different to the susceptible recurrent parent, B73 and which were carrying at least one of the teosinte‐derived resistance alleles were used to develop F2:3 populations by crossing each to B73 followed by two rounds of self‐pollination. These F2:3 populations were evaluated for SLB resistance and genotyped at the loci of interest. In 13 of 19 cases single marker analysis validated allelic substitution effects predicted from the original NIL population analysis, while in five cases we were not able to validate the effects and in one case a significant effect was detected in the opposite to the predicted direction. An allele at the QTL in bin 2.04 was shown to confer resistance to both SLB and a second maize foliar disease, gray leaf spot (GLS).}, number={4}, journal={Crop Science}, publisher={Wiley}, author={Lennon, Jill R. and Krakowsky, Matthew and Goodman, Major and Flint‐Garcia, Sherry and Balint‐Kurti, Peter J.}, year={2017}, month={May}, pages={1973–1983} }
 @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{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={0011-183X}, url={http://dx.doi.org/10.2135/cropsci2014.07.0468}, DOI={10.2135/cropsci2014.07.0468}, abstractNote={ABSTRACTGray leaf spot (GLS; causal agent Cercospora zeae‐maydis and Cercospora zeina) is an important maize (Zea mays L.) disease in the United States. Current control methods for GLS include using resistant cultivars, crop rotation, chemical applications, and conventional tillage to reduce inoculum levels. Teosinte (Z. mays subsp. parviglumis) is the wild progenitor of maize and easily forms hybrids with current maize inbreds. The aims of this study were to identify alleles from teosinte that, when introduced into temperate maize germplasm, conferred significant levels of GLS resistance. A population of 693 BC4S2 near isogenic lines (NILs), developed by crossing nine different teosinte accessions into the background of the maize inbred B73, were evaluated for GLS resistance in replicated field trials over 2 yr. Six markers significantly associated with GLS resistance were identified using 768 single nucleotide polymorphism (SNP) markers used to genotype this population. Twenty‐seven individual NILs that differed significantly from B73 for GLS resistance and that carried teosinte introgressions at the significantly associated SNPs at bins 2.04, 3.06, 4.07, 5.03, 8.06, and 9.03 were selected for follow‐up studies. F2:3 populations were developed by crossing each selected NIL to B73 followed by self‐pollinating the progeny twice. These F2:3 populations were evaluated for GLS resistance and genotyped at the loci of interest. In most cases, single‐marker analysis validated predicted allelic substitution effects from the original NIL populations.}, number={1}, journal={Crop Science}, publisher={Wiley}, author={Lennon, Jill R. and Krakowsky, Matthew and Goodman, Major and Flint-Garcia, Sherry and Balint-Kurti, Peter J.}, year={2016}, month={Jan}, pages={209–218} }
 @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}, abstractNote={Maize inbred lines NC292 and NC330 were derived by repeated backcrossing of an elite source of southern leaf blight (SLB) resistance (NC250P) to the SLB-susceptible line B73, with selection for SLB resistance among and within backcross families at each generation. Consequently, while B73 is very SLB susceptible, its sister lines NC292 and NC330 are both SLB resistant. Previously, we identified the 12 introgressions from NC250P that differentiate NC292 and NC330 from B73. The goals of this study were to determine the effects of each introgression on resistance to SLB and to two other foliar fungal diseases of maize, northern leaf blight and gray leaf spot. This was achieved by generating and testing a set of near isogenic lines carry single or combinations of just two or three introgressions in a B73 background. Introgressions 3B, 6A, and 9B (bins 3.03-3.04, 6.01, and 9.02-9.03) all conferred significant levels of SLB resistance in the field. Introgression 6A was the only introgression that had a significant effect on juvenile plant resistance to SLB. Introgressions 6A and 9B conferred resistance to multiple diseases.}, 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={GT603 (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 flavus Link:Fr. GT603 was initially selected from early self‐pollinated lines under the experimental name GT‐P50. Laboratory and field studies demonstrated that GT603 had aflatoxin 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 aflatoxin 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 aflatoxin accumulation by Aspergillus flavus (Link:Fr) has caused significant economic losses for farmers in the U.S. over the past 30 years. Aflatoxin outbreaks are generally associated with high temperatures and low moisture levels common to the southern U.S. To identify aflatoxin accumulation resistance quantitative trait loci (QTL) and linked markers for marker‐assisted breeding (MAB), a genetic mapping population of F2:3 family genotypes, increased by sib‐mating, was developed from Mp717, a maize inbred resistant to aflatoxin 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. flavus inoculation in Tifton, GA and Starkville, MS in 2004 and 2005. Quantitative trait loci on all chromosomes, except chromosomes 4, 6, and 9, were identified, and individual QTL explained from less than 1% to a maximum of 11% of the phenotypic variance in aflatoxin accumulation in grain. Both Mp717 and NC300 were found to contribute resistance to aflatoxin accumulation in the F2:3 families and overall QTL effects differed because of environmental conditions. Many of these loci were distinct from previously identified QTL, which confirmed Mp717 as a novel source of aflatoxin 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} }