Hybrid seed incompatibility in Capsella is connected to chromatin condensation defects in the endosperm

AbstractHybridization of closely related plant species is frequently connected to endosperm arrest and seed failure, for reasons that remain to be identified. In this study, we investigated the molecular events accompanying seed failure in hybrids of the closely related species pair Capsella rubella and C. grandiflora. Mapping of QTLs for the underlying cause of hybrid incompatibility in Capsella revealed three QTLs that were close to pericentromeric regions. This prompted us to investigate whether there are specific changes in heterochromatin associated with interspecific hybridizations. Indeed, we found that chromatin was less condensed in the endosperm, while the embryo was not affected. Loss of chromosome condensation was connected with a strong loss of CHG and CHH methylation and mitotic abnormalities. Genome-wide sequencing of hybrid endosperm revealed that the chromosome loss was random and was likely a consequence of reduced chromatin condensation. Consistent with reduced DNA methylation in hybrid endosperm, we found a disproportionate deregulation of genes located close to pericentromeric regions. Among those deregulated genes there were many potential targets of the AGAMOUS-LIKE transcription factor PHERES1, suggesting that reduced DNA methylation allows PHERES1 to hyperactivate its targets. Since the identified QTLs were also associated with pericentromeric regions, we conclude that relaxation of heterochromatin in response to interspecies hybridization exposes and activates loci leading to hybrid seed failure.

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Hybrid seed incompatibility in Capsella is connected to chromatin condensation defects in the endosperm

PLoS Genetics ◽

10.1371/journal.pgen.1009370 ◽

2021 ◽

Vol 17 (2) ◽

pp. e1009370

Author(s):

Katarzyna Dziasek ◽

Lauriane Simon ◽

Clément Lafon-Placette ◽

Benjamin Laenen ◽

Cecilia Wärdig ◽

...

Keyword(s):

Dna Methylation ◽

Chromatin Condensation ◽

Hybrid Seed ◽

Closely Related Species ◽

Single Chromosome ◽

Hybrid Incompatibility ◽

Molecular Events ◽

Interspecies Hybridization ◽

Capsella Rubella ◽

Related Plant

Hybridization of closely related plant species is frequently connected to endosperm arrest and seed failure, for reasons that remain to be identified. In this study, we investigated the molecular events accompanying seed failure in hybrids of the closely related species pair Capsella rubella and C. grandiflora. Mapping of QTL for the underlying cause of hybrid incompatibility in Capsella identified three QTL that were close to pericentromeric regions. We investigated whether there are specific changes in heterochromatin associated with interspecific hybridizations and found a strong reduction of chromatin condensation in the endosperm, connected with a strong loss of CHG and CHH methylation and random loss of a single chromosome. Consistent with reduced DNA methylation in the hybrid endosperm, we found a disproportionate deregulation of genes located close to pericentromeric regions, suggesting that reduced DNA methylation allows access of transcription factors to targets located in heterochromatic regions. Since the identified QTL were also associated with pericentromeric regions, we propose that relaxation of heterochromatin in response to interspecies hybridization exposes and activates loci leading to hybrid seed failure.

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The Bright and Dark Side of DNA Methylation: A Matter of Balance

Cells ◽

10.3390/cells8101243 ◽

2019 ◽

Vol 8 (10) ◽

pp. 1243 ◽

Cited By ~ 2

Author(s):

Marta Borchiellini ◽

Simone Ummarino ◽

Annalisa Di Ruscio

Keyword(s):

Dna Methylation ◽

Developmental Stages ◽

Germ Line ◽

Dark Side ◽

Epigenetic Mark ◽

Cellular Processes ◽

Biological Responses ◽

Molecular Events ◽

Genome Wide ◽

Health Related

DNA methylation controls several cellular processes, from early development to old age, including biological responses to endogenous or exogenous stimuli contributing to disease transition. As a result, minimal DNA methylation changes during developmental stages drive severe phenotypes, as observed in germ-line imprinting disorders, while genome-wide alterations occurring in somatic cells are linked to cancer onset and progression. By summarizing the molecular events governing DNA methylation, we focus on the methods that have facilitated mapping and understanding of this epigenetic mark in healthy conditions and diseases. Overall, we review the bright (health-related) and dark (disease-related) side of DNA methylation changes, outlining how bulk and single-cell genomic analyses are moving toward the identification of new molecular targets and driving the development of more specific and less toxic demethylating agents.

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Distinct pancreatic and neuronal Lung Carcinoid molecular subtypes revealed by integrative omic analysis

10.1101/2021.07.27.21260865 ◽

2021 ◽

Author(s):

Clara Domingo-Sabugo ◽

Saffron A G Willis-Owen ◽

Amit Mandal ◽

Anca Nastase ◽

Sarah Dwyer ◽

...

Keyword(s):

Dna Methylation ◽

Low Grade ◽

Single Nucleotide ◽

Neuronal Markers ◽

Molecular Events ◽

Genome Wide ◽

Whole Exome ◽

Lung Malignancies ◽

Group 2 ◽

Altered Gene

Lung Carcinoids (L-CDs) are uncommon low-grade neuroendocrine tumours that are only recently becoming characterised at the molecular level. Notably data on the molecular events that precipitate altered gene expression programmes are very limited. Here we have identified two discrete L-CD subtypes from transcriptomic and whole-genome DNA methylation data, and comprehensively defined their molecular profiles using Whole-Exome Sequencing (WES) and Single Nucleotide Polymorphism (SNP) genotyping. Subtype (Group) 1 features upregulation of neuronal markers (L-CD-NeU) and is characterised by focal spindle cell morphology, peripheral location (71%), high mutational load (P=3.4x10-4), recurrent copy number alterations and is enriched for Atypical Lung Carcinoids. Group 2 (L-CD-PanC) are centrally located and feature upregulation of pancreatic and metabolic pathway genes concordant with promoter hypomethylation of beta cell and genes related to insulin secretion (P<1x10-6). L-CD-NeU tumours harbour mutations in chromatin remodelling and in SWI/SNF complex members, while L-CD-PanC tumours show aflatoxin mutational signatures and significant DNA methylation loss genome-wide, particularly enriched in repetitive elements (P<2.2 x 10-16). Our findings provide novel insights into the distinct mechanisms of epigenetic dysregulation in these lung malignancies, potentially opening new avenues for biomarker selection and treatment in L-CD patients.

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