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Paternal chromosome loss and metabolic crisis contribute to hybrid inviability in Xenopus

ABSTRACT: Paternal chromosome loss and metabolic crisis contribute to hybrid inviability in Xenopus

OTHER RELATED OMICS DATASETS IN: GSE106157

PROVIDER: PRJNA415788 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6216950_1.fastq.gz	Fastqsanger.gz
	SRR6216950_2.fastq.gz	Fastqsanger.gz
	SRR6216951_1.fastq.gz	Fastqsanger.gz
	SRR6216951_2.fastq.gz	Fastqsanger.gz
	SRR6216952_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Paternal chromosome loss and metabolic crisis contribute to hybrid inviability in Xenopus

Project description:Hybridization of eggs and sperm from closely related species can give rise to genetic diversity, or can lead to embryo inviability due to incompatibility. Although central to evolution, the cellular and molecular mechanisms underlying postzygotic barriers that drive reproductive isolation and speciation remain largely unknown. Species of the African Clawed frog Xenopus provide an ideal system to study hybridization and genome evolution. Xenopus laevis is an allotetraploid with 36 chromosomes that arose through interspecific hybridization of diploid progenitors, whereas Xenopus tropicalis is a diploid with 20 chromosomes that diverged from a common ancestor ~48 million years ago. Differences in genome size between the two species are accompanied by organism size differences, and size scaling of the egg and subcellular structures such as nuclei and spindles formed in egg extracts. Nevertheless, early development transcriptional programs, gene expression patterns, and protein sequences are generally conserved. Interestingly, whereas the hybrid produced when X. laevis eggs are fertilized by X. tropicalis sperm (le×ts) is viable, the reverse hybrid (te×ls) dies prior to gastrulation. Here, we applied cell biological tools and high-throughput methods to study the mechanisms underlying hybrid inviability. We reveal that two specific X. laevis chromosomes are incompatible with the X. tropicalis cytoplasm and are mis-segregated during mitosis, leading to unbalanced gene expression at the maternal to zygotic transition, followed by cell-autonomous catastrophic embryo death.

2017-11-01 | GSE106157 | GEO

Paternal chromosome loss and metabolic crisis contribute to hybrid inviability in Xenopus.

Project description:Hybridization of eggs and sperm from closely related species can give rise to genetic diversity, or can lead to embryo inviability owing to incompatibility. Although central to evolution, the cellular and molecular mechanisms underlying post-zygotic barriers that drive reproductive isolation and speciation remain largely unknown. Species of the African clawed frog Xenopus provide an ideal system to study hybridization and genome evolution. Xenopus laevis is an allotetraploid with 36 chromosomes that arose through interspecific hybridization of diploid progenitors, whereas Xenopus tropicalis is a diploid with 20 chromosomes that diverged from a common ancestor approximately 48 million years ago. Differences in genome size between the two species are accompanied by organism size differences, and size scaling of the egg and subcellular structures such as nuclei and spindles formed in egg extracts. Nevertheless, early development transcriptional programs, gene expression patterns, and protein sequences are generally conserved. Whereas the hybrid produced when X. laevis eggs are fertilized by X. tropicalis sperm is viable, the reverse hybrid dies before gastrulation. Here we apply cell biological tools and high-throughput methods to study the mechanisms underlying hybrid inviability. We reveal that two specific X. laevis chromosomes are incompatible with the X. tropicalis cytoplasm and are mis-segregated during mitosis, leading to unbalanced gene expression at the maternal to zygotic transition, followed by cell-autonomous catastrophic embryo death. These results reveal a cellular mechanism underlying hybrid incompatibility that is driven by genome evolution and contributes to the process by which biological populations become distinct species.

| S-EPMC5988642 | biostudies-literature

Project description:Paternal chromosome loss and metabolic crisis contribute to hybrid inviability in Xenopus

| PRJNA417159 | ENA

Single-cell sequencing of PBMCs from myasthenia crisis patients

Project description:This project contains pre-processed single-cell sequencing data of the human peripheral blood mononuclear cells (PBMCs) from three myasthenia crisis patinets.

2023-01-13 | GSE222427 | GEO

Paternal overdiet drives intergenerational transmission of metabolic disorders through sperm epigenetic alteration [RNA-Seq]

Project description:We used a mouse model of paternal famine to simulate famine, our data show that paternal famine increases the susceptibility to metabolic disease in offspring through gametic epigenetic alterations.

2019-06-12 | GSE132521 | GEO

Paternal overdiet drives intergenerational transmission of metabolic disorders through sperm epigenetic alteration [MeDIP-Seq]

Project description:We using a mouse model of paternal famine to simulate famine, our data show that paternal famine increases the susceptibility to metabolic disease in offspring through gametic epigenetic alterations.

2019-06-13 | GSE132612 | GEO

Xenopus

Project description:Xenopus overview

| PRJNA190717 | ENA

Paternal chronic folate supplementation induced transgenerational inheritance of acquired developmental and metabolic changes in chickens

Project description:Increasing evidence indicates that the paternal diet can result in offspring metabolic changes. A proposed mechanism for paternal transmission of environmental information is via the sperm noncoding RNAs, but the definite mechanism remains unclear in birds.

2018-11-21 | GSE122759 | GEO

Xenopus laevis x Xenopus muelleri

Project description:Xenopus laevis x Xenopus muelleri overview

| PRJNA113901 | ENA

Genetic-epigenetic interactions in paternal transgenerational inheritance of metabolic disorders

Project description:Parental environmental exposures can strongly influence descendant risks for adult disease. Metabolic disorders arise from the intersection of environmental and genetic risk factors, with epigenetic inheritance being at the center of the familial cycle of transgenerational disease. How paternal high-fat diet changes the sperm chromatin leading to the acquisition of metabolic disease in offspring remains controversial and ill-defined. Using a genetic model of epigenetic inheritance, we investigated the role of histone H3 lysine 4 methylation (H3K4me3) in the paternal transmission of metabolic dysfunction. We show that obesity-induced alterations in sperm H3K4me3 associated with offspring phenotypes and corresponded to embryonic and placental chromatin profiles and gene expression. Transgenerational susceptibility to metabolic disease was only observed when grandsires had a pre-existing genetic predisposition to metabolic dysfunction that was associated with enhanced alterations to sperm H3K4me3. This non-DNA based knowledge of inheritance has the potential to improve our understanding of how environment shapes heritability and may lead to novel routes for the prevention of disease.

2022-03-30 | GSE178096 | GEO

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