scholarly journals Genetic basis of kernel nutritional traits during maize domestication and improvement

2019 ◽  
Vol 101 (2) ◽  
pp. 278-292 ◽  
Author(s):  
Hui Fang ◽  
Xiuyi Fu ◽  
Yuebin Wang ◽  
Jing Xu ◽  
Haiying Feng ◽  
...  
2018 ◽  
Author(s):  
Anne Lorant ◽  
Jeffrey Ross-Ibarra ◽  
Maud Tenaillon

Maize is an excellent model for the study of plant adaptation. Indeed, post domestication maize quickly adapted to a host of new environments across the globe. And work over the last decade has begun to highlight the role of the wild relatives of maize – the teosintes Zea mays ssp. parviglumis and ssp. mexicana – as excellent models for dissecting long-term local adaptation. Although human-driven selection associated with maize domestication has been extensively studied, the genetic bases of natural variation is still poorly understood. Here we review studies on the genetic basis of adaptation and plasticity in maize and its wild relatives. We highlight a range of different processes that contribute to adaptation and discuss evidence from natural, cultivated, and experimental populations. From an applied perspective, understanding the genetic bases of adaptation and the contribution of plasticity will provide us with new tools to both better understand and mitigate the effect of climate changes on natural and cultivated populations.


2018 ◽  
Author(s):  
Anne Lorant ◽  
Jeffrey Ross-Ibarra ◽  
Maud Tenaillon

Maize is an excellent model for the study of plant adaptation. Indeed, post domestication maize quickly adapted to a host of new environments across the globe. And work over the last decade has begun to highlight the role of the wild relatives of maize – the teosintes Zea mays ssp. parviglumis and ssp. mexicana – as excellent models for dissecting long-term local adaptation. Although human-driven selection associated with maize domestication has been extensively studied, the genetic bases of natural variation is still poorly understood. Here we review studies on the genetic basis of adaptation and plasticity in maize and its wild relatives. We highlight a range of different processes that contribute to adaptation and discuss evidence from natural, cultivated, and experimental populations. From an applied perspective, understanding the genetic bases of adaptation and the contribution of plasticity will provide us with new tools to both better understand and mitigate the effect of climate changes on natural and cultivated populations.


2021 ◽  
Author(s):  
Zhengjie Chen ◽  
Kun Hu ◽  
Yong Yin ◽  
Dengguo Tang ◽  
Jixing Ni ◽  
...  

Abstract Maize ear carries paired spikelets, whereas the ear of its wild ancestor, teosinte, bears single spikelets. However, little is known about the genetic basis of the processes of transformation of single spikelets in teosinte ear to paired spikelets in maize ear. In this study, a two-ranked, paired-spikelets primitive maize and a two-ranked, single-spikelet teosinte were utilized to develop an F2 population, and QTL mapping for single vs. paired spikelets (PEDS) was performed. Two QTL (qPEDS1.1 and qPEDS3.1) for PEDS located on chromosomes 1L and 3S were identified in the 162 F2 plants using the inclusive composite interval mapping of additive (ICIM-ADD) module, explaining 1.93% and 23.79% of the phenotypic variance, respectively. Out of the 409 F2 plants, 43 plants with PEDS = 0% and 43 plants with PEDS > 20% were selected for selective genotyping; the QTL (qPEDS3.1) accounting for 64.01% of the phenotypic variance for PEDS was also detected. Moreover, the QTL (qPEDS3.1) was validated in three environments, which explained 31.05%, 38.94% and 23.16% of the phenotypic variance, respectively. In addition, 50 epistatic QTLs were detected in 162 F2 plants using the two-locus epistatic QTL (ICIM-EPI) module; they were distributed on all 10 chromosomes and explained 94.40% of the total phenotypic variance. The results contribute to a better understanding of the genetic basis of domestication of paired spikelets and provide a genetic resource for future map-based cloning; in addition, the systematic dissection of epistatic interactions underlies a theoretical framework for overcoming epistatic effects on QTL fine mapping.


2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Zhengjie Chen ◽  
Dengguo Tang ◽  
Kun Hu ◽  
Lei Zhang ◽  
Yong Yin ◽  
...  

Abstract Background Teosinte ear bears single spikelet, whereas maize ear bears paired spikelets, doubling the number of grains in each cupulate during maize domestication. In the past 20 years, genetic analysis of single vs. paired spikelets (PEDS) has been stagnant. A better understanding of genetic basis of PEDS could help fine mapping of quantitative trait loci (QTL) and cloning of genes. Results In this study, the advanced mapping populations (BC3F2 and BC4F2) of maize × teosinte were developed by phenotypic recurrent selection. Four genomic regions associated with PEDS were detected using QTL-seq, located on 194.64–299.52 Mb, 0–162.80 Mb, 12.82–97.17 Mb, and 125.06–157.01 Mb of chromosomes 1, 3, 6, and 8, respectively. Five QTL for PEDS were identified in the regions of QTL-seq using traditional QTL mapping. Each QTL explained 1.12–38.05% of the phenotypic variance (PVE); notably, QTL qPEDS3.1 with the average PVE of 35.29% was identified in all tests. Moreover, 14 epistatic QTL were detected, with the total PVE of 47.57–66.81% in each test. The QTL qPEDS3.1 overlapped with, or was close to, one locus of 7 epistatic QTL. Near-isogenic lines (NILs) of QTL qPEDS1.1, qPEDS3.1, qPEDS6.1, and qPEDS8.1 were constructed. All individuals of NIL-qPEDS6.1(MT1) and NIL-qPEDS8.1(MT1) showed paired spikelets (PEDS = 0), but the flowering time was 7 days shorter in the NIL-qPEDS8.1(MT1). The ratio of plants with PEDS > 0 was low (1/18 to 3/18) in the NIL-qPEDS1.1(MT1) and NIL-qPEDS3.1(MT1), maybe due to the epistatic effect. Conclusion Our results suggested that major QTL, minor QTL, epistasis and photoperiod were associated with the variation of PEDS, which help us better understand the genetic basis of PEDS and provide a genetic resource for fine mapping of QTL.


2018 ◽  
Author(s):  
Markus G Stetter ◽  
Kevin Thornton ◽  
Jeffrey Ross-Ibarra

ABSTRACTUnderstanding the genetic basis of phenotypic adaptation to changing environments is an essential goal of population and quantitative genetics. While technological advances now allow interrogation of genome-wide genotyping data in large panels, our understanding of the process of polygenic adaptation is still limited. To address this limitation, we use extensive forward-time simulation to explore the impacts of variation in demography, trait genetics, and selection on the rate and mode of adaptation and the resulting genetic architecture. We simulate a population adapting to an optimum shift, modeling sequence variation for 20 QTL for each of 12 different demographies for 100 different traits varying in the effect size distribution of new mutations, the strength of stabilizing selection, and the contribution of the genomic background. We then use random forest regression approaches to learn the relative importance of input parameters in determining a number of aspects of the process of adaptation including the speed of adaptation, the relative frequency of hard sweeps and sweeps from standing variation, or the final genetic architecture of the trait. We find that selective sweeps occur even for traits under relatively weak selection and where the genetic background explains most of the variation. Though most sweeps occur from variation segregating in the ancestral population, new mutations can be important for traits under strong stabilizing selection that undergo a large optimum shift. We also show that population bottlenecks and expansion impact overall genetic variation as well as the relative importance of sweeps from standing variation and the speed with which adaptation can occur. We then compare our results to two traits under selection during maize domestication, showing that our simulations qualitatively recapitulate differences between them. Overall, our results underscore the complex population genetics of individual loci in even relatively simple quantitative trait models, but provide a glimpse into the factors that drive this complexity and the potential of these approaches for understanding polygenic adaptation.Author summaryMany traits are controlled by a large number of genes, and environmental changes can lead to shifts in trait optima. How populations adapt to these shifts depends on a number of parameters including the genetic basis of the trait as well as population demography. We simulate a number of trait architectures and population histories to study the genetics of adaptation to distant trait optima. We find that selective sweeps occur even in traits under relatively weak selection and our machine learning analyses find that demography and the effect sizes of mutations have the largest influence on genetic variation after adaptation. Maize domestication is a well suited model for trait adaptation accompanied by demographic changes. We show how two example traits under a maize specific demography adapt to a distant optimum and demonstrate that polygenic adaptation is a well suited model for crop domestication even for traits with major effect loci.


1996 ◽  
Vol 16 (02) ◽  
pp. 114-138 ◽  
Author(s):  
R. E. Scharf

SummarySpecific membrane glycoproteins (GP) expressed by the megakaryocyte-platelet system, including GPIa-lla, GPIb-V-IX, GPIIb-llla, and GPIV are involved in mediat-ing platelet adhesion to the subendothelial matrix. Among these glycoproteins, GPIIb-llla plays a pivotal role since platelet aggregation is exclusively mediated by this receptor and its interaction with soluble macromolecular proteins. Inherited defects of the GPIIb-llla or GPIb-V-IX receptor complexes are associated with bleeding disorders, known as Glanzmann's thrombasthenia, Bernard-Soulier syndrome, or platelet-type von Willebrand's disease, respectively. Using immuno-chemical and molecular biology techniques, rapid advances in our understanding of the molecular genetic basis of these disorders have been made during the last few years. Moreover, analyses of patients with congenital platelet membrane glycoprotein abnormalities have provided valuable insights into molecular mechanisms that are required for structural and functional integrity, normal biosynthesis of the glycoprotein complexes and coordinated membrane expression of their constituents. The present article reviews the current state of knowledge of the major membrane glycoproteins in health and disease. The spectrum of clinical bleeding manifestations and established diagnostic criteria for each of these dis-orders are summarized. In particular, the variety of molecular defects that have been identified so far and their genetic basis will be discussed.


Author(s):  
Deirdre O'Sullivan ◽  
Michael Moore ◽  
Susan Byrne ◽  
Andreas O. Reiff ◽  
Susanna Felsenstein

AbstractAcute disseminated encephalomyelitis in association with extensive longitudinal transverse myelitis is reported in a young child with positive anti-myelin oligodendrocyte glycoprotein (MOG) antibody with heterozygous NLRP3 missense mutations; p.(Arg488Lys) and p.(Ser159Ile). This case may well present an exceptional coincidence, but may describe a yet unrecognized feature of the spectrum of childhood onset cryopyrinopathies that contribute to the understanding of the genetic basis for anti-MOG antibody positive encephalomyelitis. Based on this observation, a larger scale study investigating the role of NLRP3 and other inflammasomes in this entity would provide important pathophysiological insights and potentially novel avenues for treatment.


Author(s):  
Lindsey Andrews ◽  
Jonathan M. Metzl

On 26 April 2013, the Wall Street Journal published an essay by neurocriminologist Adrian Raine promoting his newest book, The Anatomy of Violence: The Biological Roots of Crime. On the newspaper’s website, an image of a black-and-white brain scan overlaid with handcuffs headed the essay. Clicking ‘play’ turned the image into a video filled with three-dimensional brain illustrations and Raine’s claims that some brains are simply more biologically prone to violence than others. Rejecting what he describes as ‘the dominant model for understanding criminal behaviour in the twentieth century’ – a model based ‘almost exclusively on social and sociological’ explanations – Raine wrote that ‘the genetic basis of criminal behaviour is now well established’ through molecular and behavioural genetics.


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