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Developmental phenomics suggests that H3K4 monomethylation confers multi-level phenotypic robustness

ABSTRACT: How epigenetic modulators of gene regulation affect the development of animals has been difficult to ascertain. Despite the widespread presence of histone 3 lysine 4 monomethylation (H3K4me1) on enhancers, hypomethylation appears to have minor effects on phenotype and viability. In this study, we performed quantitative and unbiased measurements of key phenotypes in Drosophila melanogaster. Genetically induced hypomethylation reduced transcription factor enrichment in nuclear microenvironments, leading to disrupted gene expression and reduced phenotypic robustness in response to temperature changes. Our developmental phenomics approach further showed widespread, but environmentally and genetically dependent, changes in morphology, metabolism, behavior, and offspring production. Therefore, quantitative phenomics measurements under conditions resembling the natural environments of a species could unravel how pleiotropic modulators of gene expression contribute to developmental robustness. This submission contains the imaging files (confocal imaging and cuticle preparations) of the study.

ORGANISM(S): Drosophila melanogaster (fruit fly)

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PROVIDER: S-BIAD562 | bioimages |

REPOSITORIES: bioimages

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Project description:Accumulating evidence has revealed unexpected phenotypic heterogeneity and diverse functions of neutrophils in several diseases. Coronavirus disease (COVID-19) can alter the leukocyte phenotype based on disease severity, including neutrophil activation in severe cases. However, the plasticity of neutrophil phenotypes and their relative impact on COVID-19 pathogenesis has not been well addressed. This study aimed to identify and validate the heterogeneity of neutrophils in COVID-19 and evaluate the functions of each subpopulation. We analyzed public single-cell RNA-seq, bulk RNA-seq, and proteome data from healthy donors and patients with COVID-19 to investigate neutrophil subpopulations and their response to disease pathogenesis. We identified eight neutrophil subtypes: pro-neutrophil, pre-neutrophil, immature neutrophil, and five mature neutrophil subpopulations. The subtypes exhibited distinct features, including diverse activation signatures and multiple enriched pathways. The pro-neutrophil subtype was associated with severe and fatal disease, while the pre-neutrophil subtype was particularly abundant in mild/moderate disease. One of the mature neutrophil subtypes showed consistently large fractions in patients with different disease severity. Bulk RNA-seq dataset analyses using a cellular deconvolution approach validated the relative abundances of neutrophil subtypes and the expansion of pro-neutrophils in severe COVID-19 patients. Cell-cell communication analysis revealed representative ligand-receptor interactions among the identified neutrophil subtypes. Further investigation into transcription factors and differential protein abundance revealed the regulatory network differences between healthy donors and patients with severe COVID-19. Overall, we demonstrated the complex interactions among heterogeneous neutrophil subtypes and other blood cell types during COVID-19 disease. Our work has great value in terms of both clinical and public health as it furthers our understanding of the phenotypic and functional heterogeneity of neutrophils and other cell populations in multiple diseases.

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Developmental phenomics suggests that H3K4 monomethylation confers multi-level phenotypic robustness

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