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Paternal imprinting of dosage-effect defective1 contributes to seed weight xenia in maize

ABSTRACT: Paternal imprinting of dosage-effect defective1 contributes to seed weight xenia in maize

PROVIDER: PRJNA759897 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15703021_1.fastq.gz	Fastqsanger.gz
	SRR15703021_2.fastq.gz	Fastqsanger.gz
	SRR15703022_1.fastq.gz	Fastqsanger.gz
	SRR15703022_2.fastq.gz	Fastqsanger.gz
	SRR15703023_1.fastq.gz	Fastqsanger.gz

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Paternal imprinting of dosage-effect defective1 contributes to seed weight xenia in maize.

Project description:Historically, xenia effects were hypothesized to be unique genetic contributions of pollen to seed phenotype, but most examples represent standard complementation of Mendelian traits. We identified the imprinted dosage-effect defective1 (ded1) locus in maize (Zea mays) as a paternal regulator of seed size and development. Hypomorphic alleles show a 5-10% seed weight reduction when ded1 is transmitted through the male, while homozygous mutants are defective with a 70-90% seed weight reduction. Ded1 encodes an R2R3-MYB transcription factor expressed specifically during early endosperm development with paternal allele bias. DED1 directly activates early endosperm genes and endosperm adjacent to scutellum cell layer genes, while directly repressing late grain-fill genes. These results demonstrate xenia as originally defined: Imprinting of Ded1 causes the paternal allele to set the pace of endosperm development thereby influencing grain set and size.

| S-EPMC9470594 | biostudies-literature

Paternal imprinting of dosage-effect defective1 contributes to seed weight xenia in maize

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-06-10 | GSE183304 | GEO

Polycomb-mediated repression of paternal chromosomes maintains haploid dosage in diploid embryos of Marchantia [RNA-seq]

Project description:Complex mechanisms regulate gene dosage throughout eukaryotic life cycles. Mechanisms controlling gene dosage have been extensively studied in animals, however it is unknown how generalizable these mechanisms are to diverse eukaryotes. Here, we use the haploid plant Marchantia polymorpha to assess gene dosage control in its short-lived diploid embryo. We show that throughout embryogenesis, paternal chromosomes are repressed resulting in functional haploidy. The paternal genome is targeted for genomic imprinting by the Polycomb mark H3K27me3 starting at fertilization, rendering the maternal genome in control of embryogenesis. Maintaining haploid gene dosage by this new form of imprinting is essential for embryonic development. Our findings illustrate how haploid-dominant species can regulate gene dosage through paternal chromosome inactivation and initiates the exploration of the link between life cycle history and gene dosage in a broader range of organisms.

2022-08-23 | GSE193306 | GEO

Polycomb-mediated repression of paternal chromosomes maintains haploid dosage in diploid embryos of Marchantia [CUT&RUN]

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Maternal care boosted by paternal imprinting in mammals

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Paternally-acting canonical RNA-directed DNA methylation pathway genes sensitizes Arabidopsis endosperm to paternal dosage [RNA-Seq]

Project description:Seed development is sensitive to parental dosage, with excess maternal or paternal genomes creating reciprocal phenotypes. Paternal genomic excess results in extensive endosperm proliferation without cellularization and eventual seed abortion. We previously showed that loss of the RNA POL IV gene nrpd1 in tetraploid fathers represses seed abortion in paternal excess crosses. Here we show genetically that RNA-directed DNA methylation (RdDM) pathway activity in the paternal parent is sufficient to determine the viability of paternal excess seeds. The status of the RdDM pathway in paternal excess endosperm does not impact seed viability. Comparison of endosperm transcriptomes, DNA methylation, and small RNAs from balanced and paternal excess endosperm demonstrates that paternal excess seed abortion is unlikely to be dependent on either transposable element or imprinted gene mis-regulation. We suggest instead that loss of paternal RdDM modulates expression at a small subset of genes and desensitizes endosperm to paternal excess. Finally, using allele-specific transcription data, we present evidence of a transcriptional buffering system that up37 regulates maternal alleles and represses paternal alleles in response to excess paternal genomic dosage. These findings prompt reconsideration of models for dosage sensitivity in endosperm.

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Paternally-acting canonical RNA-directed DNA methylation pathway genes sensitizes Arabidopsis endosperm to paternal dosage [Bisulfite-seq]

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Paternally-acting canonical RNA-directed DNA methylation pathway genes sensitizes Arabidopsis endosperm to paternal dosage [miRNA-Seq]

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