15 research outputs found

    Genome-wide association study of quality traits and starch pasting properties of maize kernels

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    Abstract Background Starch are the main nutritional components of maize (Zea mays L.), and starch pasting properties are widely used as essential indicators for quality estimation. Based on the previous studies, various genes related to pasting properties have been identified in maize. However, the loci underlying variations in starch pasting properties in maize inbred lines remain to be identified. Results To investigate the genetic architecture of these traits, the starch pasting properties were examined based on 292 maize inbred lines, which were genotyped with the MaizeSNP50 BeadChip composed of 55,126 evenly spaced, random SNPs. A genome-wide association study (GWAS) implemented in the software package FarmCPU was employed to identify genomic loci for the starch pasting properties. 48 SNPs were found to be associated with pasting properties. Moreover, 37 candidate genes were correlated with pasting properties. Among the candidate genes, GRMZM2G143646 and GRMZM2G166407 were associated with breakdown and final viscosity significantly, and both genes encode PPR (Pentatricopeptide repeat) protein. We used GWAS to explore candidate genes of maize starch pasting properties in this study. The identified candidate genes will be useful for further understanding of the genetic architecture of starch pasting properties in maize. Conclusion This study showed a complex regulation network about maize quality trait and starch pasting properties. It may provide some useful markers for marker assisted selection and a basis for cloning the genes behind these SNPs

    Construction of CoP2-Mo4P3/NF Heterogeneous Interfacial Electrocatalyst for Boosting Water Splitting

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    Developing highly efficient, cost effective and durable bifunctional electrocatalyst remains a key challenge for overall water splitting. Herein, a bifunctional catalyst CoP2-Mo4P3/NF with rich heterointerfaces was successfully prepared by a two-step hydrothermal-phosphorylation method. The synergistic interaction between CoP2 and Mo4P3 heterogeneous interfaces can optimize the electronic structure of active sites, leading to the weak adsorption of H on the Mo sites and the increased redox activity of the Co site, resultantly improving the HER/OER bifunctional catalytic activity. The synthesized CoP2-Mo4P3/NF catalyst exhibits excellent electrocatalytic activity in 1.0 M KOH with low overpotentials of 77.6 and 300.3 at 100 mA cm−2 for HER and OER, respectively. Additionally, the assembled CoP2-Mo4P3/NF||CoP2-Mo4P3/NF electrolyzer delivers a current density of 100 mA cm−2 at a cell voltage of 1.59 V and remains stable for at least 370 h at 110 mA cm−2, indicating the potential application prospective in water splitting

    Haploinsufficiency leads to neurodegeneration in C9ORF72 ALS/FTD human induced motor neurons

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    An intronic GGGGCC repeat expansion in C9ORF72 is the most common cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), but the pathogenic mechanism of this repeat remains unclear. Using human induced motor neurons (iMNs), we found that repeat-expanded C9ORF72 was haploinsufficient in ALS. We found that C9ORF72 interacted with endosomes and was required for normal vesicle trafficking and lysosomal biogenesis in motor neurons. Repeat expansion reduced C9ORF72 expression, triggering neurodegeneration through two mechanisms: accumulation of glutamate receptors, leading to excitotoxicity, and impaired clearance of neurotoxic dipeptide repeat proteins derived from the repeat expansion. Thus, cooperativity between gain- and loss-of-function mechanisms led to neurodegeneration. Restoring C9ORF72 levels or augmenting its function with constitutively active RAB5 or chemical modulators of RAB5 effectors rescued patient neuron survival and ameliorated neurodegenerative processes in both gain- and loss-of-function C9ORF72 mouse models. Thus, modulating vesicle trafficking was able to rescue neurodegeneration caused by the C9ORF72 repeat expansion. Coupled with rare mutations in ALS2, FIG4, CHMP2B, OPTN and SQSTM1, our results reveal mechanistic convergence on vesicle trafficking in ALS and FTD
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