5 research outputs found

    Linkage mapping and genomic prediction of grain quality traits in tropical maize (Zea mays L.)

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    The suboptimal productivity of maize systems in sub-Saharan Africa (SSA) is a pressing issue, with far-reaching implications for food security, nutrition, and livelihood sustainability within the affected smallholder farming communities. Dissecting the genetic basis of grain protein, starch and oil content can increase our understanding of the governing genetic systems, improve the efficacy of future breeding schemes and optimize the end-use quality of tropical maize. Here, four bi-parental maize populations were evaluated in field trials in Kenya and genotyped with mid-density single nucleotide polymorphism (SNP) markers. Genotypic (G), environmental (E) and GΓ—E variations were found to be significant for all grain quality traits. Broad sense heritabilities exhibited substantial variation (0.18–0.68). Linkage mapping identified multiple quantitative trait loci (QTLs) for the studied grain quality traits: 13, 7, 33, 8 and 2 QTLs for oil content, protein content, starch content, grain texture and kernel weight, respectively. The co-localization of QTLs identified in our research suggests the presence of shared genetic factors or pleiotropic effects, implying that specific genomic regions influence the expression of multiple grain quality traits simultaneously. Genomic prediction accuracies were moderate to high for the studied traits. Our findings highlight the polygenic nature of grain quality traits and demonstrate the potential of genomic selection to enhance genetic gains in maize breeding. Furthermore, the identified genomic regions and single nucleotide polymorphism markers can serve as the groundwork for investigating candidate genes that regulate grain quality traits in tropical maize. This, in turn, can facilitate the implementation of marker-assisted selection (MAS) in breeding programs focused on improving grain nutrient levels

    Genome-wide association studies of grain yield and quality traits under optimum and low-nitrogen stress in tropical maize (Zea mays L.)

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    Soils in sub-Saharan Africa are nitrogen deficient due to low fertilizer use and inadequate soil fertility management practices. This has resulted in a significant yield gap for the major staple crop maize, which is undermining nutritional security and livelihood sustainability across the region. Dissecting the genetic basis of grain protein, starch and oil content under nitrogen-starved soils can increase our understanding of the governing genetic systems and improve the efficacy of future breeding schemes. An association mapping panel of 410 inbred lines and four bi-parental populations were evaluated in field trials in Kenya and South Africa under optimum and low nitrogen conditions and genotyped with 259,798 SNP markers. Genetic correlations demonstrated that these populations may be utilized to select higher performing lines under low nitrogen stress. Furthermore, genotypic, environmental and GxE variations in nitrogen-starved soils were found to be significant for oil content. Broad sense heritabilities ranged from moderate (0.18) to high (0.86). Under low nitrogen stress, GWAS identified 42 SNPs linked to grain quality traits. These significant SNPs were associated with 51 putative candidate genes. Linkage mapping identified multiple QTLs for the grain quality traits. Under low nitrogen conditions, average prediction accuracies across the studied genotypes were higher for oil content (0.78) and lower for grain yield (0.08). Our findings indicate that grain quality traits are polygenic and that using genomic selection in maize breeding can improve genetic gain. Furthermore, the identified genomic regions and SNP markers can be utilized for selection to improve maize grain quality traits

    Inducible deletion of CD28 prior to secondary nippostrongylus brasiliensis infection impairs worm expulsion and recall of protective memory CD4 (+) T cell responses

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    IL-13 driven Th2 immunity is indispensable for host protection against infection with the gastrointestinal nematode Nippostronglus brasiliensis. Disruption of CD28 mediated costimulation impairs development of adequate Th2 immunity, showing an importance for CD28 during the initiation of an immune response against this pathogen. In this study, we used global CD28βˆ’/βˆ’ mice and a recently established mouse model that allows for inducible deletion of the cd28 gene by oral administration of tamoxifen (CD28βˆ’/loxCre+/βˆ’+TM) to resolve the controversy surrounding the requirement of CD28 costimulation for recall of protective memory responses against pathogenic infections. Following primary infection with N. brasiliensis, CD28βˆ’/βˆ’ mice had delayed expulsion of adult worms in the small intestine compared to wild-type C57BL/6 mice that cleared the infection by day 9 post-infection. Delayed expulsion was associated with reduced production of IL-13 and reduced serum levels of antigen specific IgG1 and total IgE. Interestingly, abrogation of CD28 costimulation in CD28βˆ’/loxCre+/βˆ’ mice by oral administration of tamoxifen prior to secondary infection with N. brasiliensis resulted in impaired worm expulsion, similarly to infected CD28βˆ’/βˆ’ mice. This was associated with reduced production of the Th2 cytokines IL-13 and IL-4, diminished serum titres of antigen specific IgG1 and total IgE and a reduced CXCR5+ TFH cell population. Furthermore, total number of CD4+ T cells and B220+ B cells secreting Th1 and Th2 cytokines were significantly reduced in CD28βˆ’/βˆ’ mice and tamoxifen treated CD28βˆ’/loxCre+/βˆ’ mice compared to C57BL/6 mice. Importantly, interfering with CD28 costimulatory signalling before re-infection impaired the recruitment and/or expansion of central and effector memory CD4+ T cells and follicular B cells to the draining lymph node of tamoxifen treated CD28βˆ’/loxCre+/βˆ’ mice. Therefore, it can be concluded that CD28 costimulation is essential for conferring host protection during secondary N. brasiliensis infection

    A Transendocytosis Perspective on the CD28/CTLA-4 Pathway

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