Search for: All records

Abstract Introducing and characterizing variation through mutagenesis plus functional genomics can accelerate resistance breeding as well as our understanding of crop plant immunity. To reveal new germplasm resources for fungal disease resistance breeding in elite durum wheat, we challenged the diverse alleles in a sequenced and cataloged ethyl methanesulfonate mutagenized population of elite tetraploid wheatTriticum turgidumsubsp.durumcv ‘Kronos’ with stripe rust. We screened 2,000 mutant lines and identified sixteen enhanced disease resistance (EDR) lines with persistent resistance to stripe rust over four years of field testing. To find broad-spectrum resistance, we challenged these lines with other major biotrophic and necrotrophic pathogens, including those causing Septoria tritici blotch, tan spot, Fusarium head blight and leaf rust. Enhanced resistance to multiple fungi was found in 13 of 16 EDR lines. Five EDR lines showed spontaneous lesion formation in the absence of pathogens, providing new mutant resources to study plant stress response in the absence of the confounding effects of pathogen infection. We mapped exome capture sequencing data of the EDR lines to a recently released long-read Kronos genome to aid in the identification of causal mutations. We located an EDR resistance locus to an 175 Mb interval on chromosome 1B. Importantly, these phenotypically characterized EDR lines are newly described durum germplasm coupled with improved functional genomics resources that are readily available for both wheat fungal resistance breeding and basic plant immunity research. 

Abstract We have examined the roles of yeast mRNA decapping-activators Pat1 and Dhh1 in repressing the translation and abundance of specific mRNAs in nutrient-replete cells using ribosome profiling, RNA-Seq, CAGE analysis of capped mRNAs, RNA Polymerase II ChIP-Seq, and TMT-mass spectrometry of mutants lacking one or both factors. Although the Environmental Stress Response (ESR) is activated in dhh1Δ and pat1Δ mutants, hundreds of non-ESR transcripts are elevated in a manner indicating cumulative repression by Pat1 and Dhh1 in wild-type cells. These mRNAs show both reduced decapping and diminished transcription in the mutants, indicating that impaired mRNA turnover drives transcript derepression in cells lacking Dhh1 or Pat1. mRNA degradation stimulated by Dhh1/Pat1 is not dictated by poor translation nor enrichment for suboptimal codons. Pat1 and Dhh1 also collaborate to reduce translation and protein production from many mRNAs. Transcripts showing concerted translational repression by Pat1/Dhh1 include mRNAs involved in cell adhesion or utilization of the poor nitrogen source allantoin. Pat1/Dhh1 also repress numerous transcripts involved in respiration, catabolism of non-preferred carbon or nitrogen sources, or autophagy; and we obtained evidence for elevated respiration and autophagy in the mutants. Thus, Pat1 and Dhh1 function as post-transcriptional repressors of multiple pathways normally activated only during nutrient limitation. 

Age at depressive onset (AAO) corresponds to unique symptomatology and clinical outcomes. Integration of genome-wide association study (GWAS) results with additional “omic” measures to evaluate AAO has not been reported and may reveal novel markers of susceptibility and/or resistance to major depressive disorder (MDD). To address this gap, we integrated genomics with metabolomics using data-driven network analysis to characterize and differentiate MDD based on AAO. This study first performed two GWAS for AAO as a continuous trait in (a) 486 adults from the Pharmacogenomic Research Network-Antidepressant Medication Pharmacogenomic Study (PGRN-AMPS), and (b) 295 adults from the Combining Medications to Enhance Depression Outcomes (CO-MED) study. Variants from top signals were integrated with 153 p180-assayed metabolites to establish multi-omics network characterizations of early (