Multi-Species Genomics-Enabled Selection for Improving Agroecosystems Across Space and Time

Plant breeding has been central to global increases in crop yields. Breeding deserves praise for helping to establish better food security, but also shares the responsibility of unintended consequences. Much work has been done describing alternative agricultural systems that seek to alleviate these externalities, however, breeding methods and breeding programs have largely not focused on these systems. Here we explore breeding and selection strategies that better align with these more diverse spatial and temporal agricultural systems

Homeologous epistasis in wheat: The search for an immortal hybrid

Supplemental file(s) description: CNLM phenotypes, CNLM SNP information, CNLM marker scores, Table of BLUPs for CNLM, Homeologous gene sets, All non-unique homeologous marker sets, Unique homeologous marker sets, Within marker sets, Across marker sets, Table of two-way interaction estimates for CNLM, Table of three-way interaction estimates for CNLM, RIL Rht-1 linked markers and plant height, LaTeX file of DissertationThe subgenomes of an allopolyploid crop will each contain complete, yet evolutionarily divergent, sets of genes. Like a diploid hybrid, allopolyploids will have two versions, or homeoalleles, for every gene. Partial functional redundancy between homeologous genes should result in a deviation from additivity. These epistatic interactions between homeoalleles are analogous to dominance effects, but are fixed across subgenomes through self pollination. An allopolyploid can therefore be viewed as an immortalized hybrid, with the opportunity to select and fix favorable homeoallelic interactions within inbred varieties. With the availability of affordable genotyping and a reference genome to locate markers, breeders of allopolyploids now have the opportunity to manipulate subgenomes independently and fix beneficial interactions across subgenomes. I present a statistical framework for partitioning genetic variance to individual subgenomes of an allopolyploid, predicting breeding values for each subgenome, and evaluating the magnitude of homeologous epistasis. I also present a subfunctionalization epistasis model to estimate the degree of functional redundancy between homeoallelic loci and to determine their importance within a population. I search for genome-wide patterns indicative of homeoallelic subfunctionalization in a winter wheat breeding population by anchoring homeologous marker sets to the IWGSC RefSeq v1.0 sequence. Some traits displayed a pattern indicative of homeoallelic subfunctionalization, while other traits showed a less clear pattern. Using genomic prediction accuracy to evaluate importance of marker interactions, I show that homeologous interactions explain a significant portion of the non-additive genetic signal. Allopolyploids have traditionally been treated as diploids in breeding programs because they undergo disomic inheritance. With modern DNA marker technology and ever increasing computational power, I provide a new framework for breeders of allopolyploid crops to characterize the genetic architecture of existing populations, determine breeding goals, and develop new strategies for selection of additive effects and homeologous epistasis in these ancient immortal hybrids

A Low Resolution Epistasis Mapping Approach To Identify Chromosome Arm Interactions in Allohexaploid Wheat

Epistasis is an important contributor to genetic variance. In inbred populations, pairwise epistasis is present as additive by additive interactions. Testing for epistasis presents a multiple testing problem as the pairwise search space for modest numbers of markers is large. Single markers do not necessarily track functional units of interacting chromatin as well as haplotype based methods do. To harness the power of multiple markers while minimizing the number of tests conducted, we present a low resolution test for epistatic interactions across whole chromosome arms. Epistasis covariance matrices were constructed from the additive covariances of individual chromosome arms. These covariances were subsequently used to estimate an epistatic variance parameter while correcting for background additive and epistatic effects. We find significant epistasis for 2% of the interactions tested for four agronomic traits in a winter wheat breeding population. Interactions across homeologous chromosome arms were identified, but were less abundant than other chromosome arm pair interactions. The homeologous chromosome arm pair 4BL/4DL showed a strong negative relationship between additive and interaction effects that may be indicative of functional redundancy. Several chromosome arms appeared to act as hubs in an interaction network, suggesting that they may contain important regulatory factors. The differential patterns of epistasis across different traits demonstrate that detection of epistatic interactions is robust when correcting for background additive and epistatic effects in the population. The low resolution epistasis mapping method presented here identifies important epistatic interactions with a limited number of statistical tests at the cost of low precision

Prediction of Subgenome Additive and Interaction Effects in Allohexaploid Wheat

Whole genome duplications have played an important role in the evolution of angiosperms. These events often occur through hybridization between closely related species, resulting in an allopolyploid with multiple subgenomes. With the availability of affordable genotyping and a reference genome to locate markers, breeders of allopolyploids now have the opportunity to manipulate subgenomes independently. This also presents a unique opportunity to investigate epistatic interactions between homeologous orthologs across subgenomes. We present a statistical framework for partitioning genetic variance to the subgenomes of an allopolyploid, predicting breeding values for each subgenome, and determining the importance of inter-genomic epistasis. We demonstrate using an allohexaploid wheat breeding population evaluated in Ithaca, NY and an important wheat dataset from CIMMYT previously shown to demonstrate non-additive genetic variance. Subgenome covariance matrices were constructed and used to calculate subgenome interaction covariance matrices for variance component estimation and genomic prediction. We propose a method to extract population structure from all subgenomes at once before covariances are calculated to reduce collinearity between subgenome estimates. Variance parameter estimation was shown to be reliable for additive subgenome effects, but was less reliable for subgenome interaction components. Predictive ability was equivalent to current genomic prediction methods. Including only inter-genomic interactions resulted in the same increase in accuracy as modeling all pairwise marker interactions. Thus, we provide a new tool for breeders of allopolyploid crops to characterize the genetic architecture of existing populations, determine breeding goals, and develop new strategies for selection of additive effects and fixation of inter-genomic epistasis

Scalable growth models for time‐series multispectral images

Abstract Vegetation indices (VIs) are produced as a combination of different reflectance bands that are captured by multispectral images (MSIs). These indices, such as normalized difference vegetation index (NDVI), are reported to be proxy indicators of photosynthetic activity, plant canopy biomass, and leaf area index. To determine the utility of using VI derived from MSI to model plant growth, random regression (RR) models with linear splines and different orders of Legendre polynomials were applied to data collected (years 2019 and 2020) as part of the Genome‐to‐Fields initiative. Growth curves of maize (Zea mays L.) hybrids were modeled using both NDVI and cumulative NDVI (cNDVI) phenotypes. Due to the difference in MSI recording dates, and sparse overlap in hybrids between years, all the analyses were nested within a year. Results indicate that RR models using Legendre polynomials provide a robust and scalable method for modeling growth curves using phenotypes extracted from MSI; however, RR models using linear splines showed inconsistent convergence. Growth curves estimated using NDVI and cNDVI showed low‐to‐moderate heritability (0.11–0.44) and a range of genetic correlations (−0.15 to 0.97) with grain yield. This study demonstrates the utility of MSI for modeling genetic growth trends, with the best modeling results obtained when using Legendre polynomials and cNDVI

Adefovir dipivoxil for wait-listed and post-liver transplantation patients with lamivudine-resistant hepatitis B: Final long-term results

Wait-listed (n = 226) or post-liver transplantation (n = 241) chronic hepatitis B (CHB) patients with lamivudine-resistant hepatitis B virus (HBV) were treated with adefovir dipivoxil for a median of 39 and 99 weeks, respectively. Among wait-listed patients, serum HBV DNA levels became undetectable (<l,000 copies/mL) in 59% and 65% at weeks 48 and 96, respectively. After 48 weeks, alanine aminotransferase (ALT), albumin, bilirubin, and prothrombin time normalized in 77%, 76%, 60%, and 84% of wait-listed patients, respectively. Among postransplantation patients, serum HBV DNA levels became undetectable in 40% and 65% at weeks 48 and 96, respectively. After 48 weeks, ALT, albumin, bilirubin, and prothrombin time normalized in 51%, 81%. 76%, and 56% of posttransplantation patients, respectively. Among wait-listed patients who underwent on-study liver transplantation, protection from graft reinfection over a median of 35 weeks was similar among parents who did (n = 34) or did not (n = 23) receive hepatitis B immunoglobulin (HBIg). Hepatitis B surface antigen was detected on the first measurement only in 6% and 9% of patiends who did or did not receive HBIg, respectively. Serum HBV DNA was detected on consecutive visits in 6% and 0% of patients who did or did not receive HBIg, respectively. Treatment-related adverse events led to discontinuation of adefovir dipivoxil in 4% of patients. Cumulative probabilities of resistance were 0%, 2%, and 2% at weeks 48, 96, and 144, respectively. In conclusion, adefovir dipivoxil is effective and safe at wait-listed or posttransplantation CHB patients with lamivudine-resistant HBV and prevents graft reinfection with or without HBIg. © 2007 AASLD

Adefovir dipivoxil for wait-listed and post-liver transplantation patients with lamivudine-resistant hepatitis B : final long-term results

Wait-listed (n = 226) or post-liver transplantation (n = 241) chronic hepatitis B (CHB) patients with lamivudine-resistant hepatitis B virus (HBV) were treated with adefovir dipivoxil for a median of 39 and 99 weeks, respectively. Among wait-listed patients, serum HBV DNA levels became undetectable (<1,000 copies/mL) in 59% and 65% at weeks 48 and 96, respectively. After 48 weeks, alanine aminotransferase (ALT), albumin, bilirubin, and prothrombin time normalized in 77%, 76%, 60%, and 84% of wait-listed patients, respectively. Among posttransplantation patients, serum HBV DNA levels became undetectable in 40% and 65% at weeks 48 and 96, respectively. After 48 weeks, ALT, albumin, bilirubin, and prothrombin time normalized in 51%, 81%, 76%, and 56% of posttransplantation patients, respectively. Among wait-listed patients who underwent on-study liver transplantation, protection from graft reinfection over a median of 35 weeks was similar among patients who did (n = 34) or did not (n = 23) receive hepatitis B immunoglobulin (HBIg). Hepatitis B surface antigen was detected on the first measurement only in 6% and 9% of patients who did or did not receive HBIg, respectively. Serum HBV DNA was detected on consecutive visits in 6% and 0% of patients who did or did not receive HBIg, respectively. Treatment-related adverse events led to discontinuation of adefovir dipivoxil in 4% of patients. Cumulative probabilities of resistance were 0%, 2%, and 2% at weeks 48, 96, and 144, respectively. In conclusion, adefovir dipivoxil is effective and safe in wait-listed or posttransplantation CHB patients with lamivudine-resistant HBV and prevents graft reinfection with or without HBIg