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Natural polymorphisms in ZMET2 encoding a DNA methyltransferase modulate the number of husk layers in maize

ABSTRACT: Natural polymorphisms in ZMET2 encoding a DNA methyltransferase modulate the number of husk layers in maize

PROVIDER: PRJNA988518 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25054800_1.fastq.gz	Fastqsanger.gz
	SRR25054800_2.fastq.gz	Fastqsanger.gz
	SRR25054801_1.fastq.gz	Fastqsanger.gz
	SRR25054801_2.fastq.gz	Fastqsanger.gz
	SRR25054802_1.fastq.gz	Fastqsanger.gz

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Natural polymorphisms in ZMET2 encoding a DNA methyltransferase modulate the number of husk layers in maize

Project description:The goals of this study are to investigate the effect of ZMET2 on genome-wide DNA methylation and gene expression.

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The RHW1-ZCN4 regulatory pathway confers natural variation of husk leaf width in maize

Project description:Maize husk leaf - the outer leafy layers covering the ear - modulates kernel yield and quality. Despite its importance, however, the genetic controls underlying husk leaf development remain elusive. Our previous genome-wide association study identified a single nucleotide polymorphism located in the gene RHW1 (Regulator of Husk leaf Width) that is significantly associated with husk leaf-width diversity in maize. Here, we further demonstrate that a polymorphic 18-bp InDel (insertion/deletion) variant in the 3' untranslated region of RHW1 alters its protein abundance and accounts for husk leaf width variation. RHW1 encodes a putative MYB-like transcriptional repressor. Disruption of RHW1 altered cell proliferation and resulted in a narrower husk leaf, whereas RHW1 overexpression yielded a wider husk leaf. RHW1 positively regulated the expression of ZCN4, a well-known TFL1-like protein involved in maize ear development. Dysfunction of ZCN4 reduced husk leaf width even in the context of RHW1 overexpression. The InDel variant in RHW1 is subject to selection and is associated with maize husk leaf adaption from tropical to temperate regions. Overall, our results identify that RHW1-ZCN4 regulates a pathway conferring husk leaf width variation at a very early stage of husk leaf development in maize.

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Project description:In the mammalian cortex, neurons and glia form a patterned structure across six layers whose complex cytoarchitectonic arrangement likely contributes greatly to cognitive abilities. We sequenced transcriptomes from layers 1-6b of the adult (P56) mouse primary somatosensory cortex, along with dorsal cortex and lateral cortex, to understand the transcriptional levels and functional repertoires of coding and noncoding loci for cells that constitute these layers. 5,835 protein-coding genes and 66 noncoding RNA loci are differentially expressed (patterned) across the layers, based on a machine-learning model (naive Bayes) approach. Layers 2-6b are each associated with specific functional and disease annotations that provide insights into their biological roles. This new resource greatly extends currently available resources, such as the Allen Mouse Brain Atlas and microarray data sets, by providing quantitative expression levels, by being genome-wide, by including novel loci, and by identifying alternatively spliced transcripts that are differentially expressed across layers.

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Population genetic properties of differentiated human copy number polymorphisms

Project description:Copy number variants (CNVs) can reach appreciable frequencies in the human population, and several of these copy number polymorphisms (CNPs) have been recently associated with human diseases including lupus, psoriasis, Crohn disease, and obesity. Despite new advances, significant biases remain in terms of CNP discovery and genotyping. Developing a novel method based on single channel intensity data and benchmarking against copy numbers determined from sequencing read-depth, we successfully obtained CNP genotypes for 1489 CNPs from 487 human DNA samples from diverse ethnic backgrounds. This customized microarray was enriched for segmental duplication-rich regions and novel insertions of sequences not represented in the reference genome assembly or on standard single nucleotide polymorphism (SNP) microarray platforms. We observe that CNPs in segmental duplications are more likely to be population differentiated than CNPs in unique regions (p = 0.015) and that bi-allelic CNPs show greater stratification when compared to frequency-matched SNPs (p = 0.0026). Although bi-allelic CNPs show a strong correlation of copy number with flanking SNP genotypes, the majority of multi-copy CNPs do not (40% with r >0.8). We selected a subset of CNPs for further characterization in 1873 additional samples from 62 populations (947 samples analyzed by microarray; 926 samples analyzed with PCR based assays); this revealed striking population-differentiated structural variants in genes of clinical significance such as the OCLN gene, a tight junction protein involved in hepatitis C viral entry. Our new microarray design allows these variants to be rapidly tested for disease association and our results suggest that CNPs (especially those that are not in linkage disequilibrium with SNPs) may have contributed disproportionately to human diversity and selection.

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