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Effects of FOXN1 or AFF4 deficiency on gene expression in the skin

ABSTRACT: Loss-of-function mutations in Foxn1 or Aff4 cause similar defects in skin morphology. To determine whether these similar phenotypes result from similar changes in gene expression, skin from wild-type, Foxn1-null, or Aff4 conditional knockout (cko) mice was analysed by RNA-seq at a time when the animals were attempting to grow their first hair coats (P6).

ORGANISM(S): Mus musculus

PROVIDER: GSE152247 | GEO | 2020/11/23

REPOSITORIES: GEO

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Effects of FOXN1 or AFF4 deficiency on gene expression in the skin

Project description:Effects of FOXN1 or AFF4 deficiency on gene expression in the skin

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Hypoxia and Foxn1 alter dermal fibroblasts proteomics signature to redirect scar-less to scar-forming skin wound healing in Foxn1-/- mice

Project description:Hypoxia is one of the factors that govern reparative vs regenerative skin wound healing. Data-independent acquisition (DIA) experiment was carried out to study the effect of hypoxia and Foxn1 on mice dermal fibroblast proteomics signature and skin wound healing of Foxn1-deficient (Foxn1-/-) mice.

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Hypoxia induces Foxn1 and Mmp-9 expression in keratinocytes: proteomics analysis of mouse keratinocytes transiently activated by Foxn1

Project description:Recent studies have shown that transcription factor Foxn1 expressed in keratinocytes is involved in skin wound healing process, yet how Foxn1 functions remains largely unknown. Proteomic analysis using a two-dimensional differential gel electrophoresis (2D-DIGE) technique coupled with MALDI-TOF/TOF was used to analyze in vitro cultured keratinocytes transfected with adenoviral vector carrying Foxn1-GFP or GFP-alone (control). Sixty-six of sixty-nine protein spots differed in abundance between compared groups were identified.

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Hypoxia reveals the new function of Foxn1 in keratinocytes antioxidant defense system

Project description:Skin exposed to environmental threats including injuries and oxidative stress developed an efficient but not fully recognized systems of repair and antioxidant protection. In this project we provide evidence that Foxn1 in keratinocytes regulates elements of electron transport chain and participates in thioredoxin system (Txn2, Txnrd3, Srxn1) induction, particularly under hypoxic environment. It is shown that Foxn1 in keratinocytes upregulate glutathione thioredoxin reductase 3 (Txnrd3) protein, and high levels of Txnrd3 mRNA were detected in injured skin of Foxn1+/+ mice. It also shown that Foxn1 strongly downregulate CCN2 protein participating in reconstruction of the epidermis after injury. As in vitro assay revealed that Foxn1 controls keratinocytes migration stimulating it under normoxia and suppressing under hypoxia. Keratinocytes overexpressing Foxn1 and exposed to hypoxia showed reduced ability to promote angiogenesis by downregulation of Vegfa. In conclusion, this study showed a new mechanism in which Foxn1, along with hypoxia, participates in the activation of antioxidant defense and controls functional properties of keratinocytes.

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Transcriptome characterization of CHOPS syndrome, a novel genetic disorder caused by gain-of-function mutations of AFF4

Project description:AFF4 is a component of super elongation complex (SEC), which plays an important role in mobilizing paused RNA polymerase II at gene promoter regions. Using exome sequenging, we have identified a novel genetic disorder caused by missense mutations in AFF4. We propose CHOPS syndrome as a name for this new diagnosis. To evaluate the effect of identified missense mutations of AFF4, utilizing patient derived skin fibroblast cell lines, the gene expression analysis was perfomred. To characterize the transcriptome pattern observed in CHOPS syndrome, the skin fibroblast samples from two CHOPS syndrome probands and three healthy control subjects were used. Samples used for expression array include two CHOPs syndrome samples (CDL160: 6 year-old Caucasian female with 254S mut and CDL444: 12 year-old Caucasian male with 254A mut) and three age gender matched controls (GM01652: 11 year-old Caucasian female, GM02036 11 year-old Caucasian female and GM08398: 8 year-old Caucasian male).

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Transcriptome characterization of CHOPS syndrome, a novel genetic disorder caused by gain-of-function mutations of AFF4

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AFF4 regulates cellular adipogenic differentiation via targeting autophagy

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Neotenic phenomenon in gene expression in the skin of Foxn1 deficient (nude) mice– projection for regenerative skin wound healing

Project description:Uninjured skin of adult C57BL/6J mice and mouse fetuses at 18 day of embryonic development (E18), as the models of reparative healing, and Nude and E14, as the models of regenerative healing, were characterized for their gene expression profiles by next-generation high-throughput DNA sequencing. The comparisons of gene expression profiles indicated that there were more similarities within each model of healing (Nude was more similar to E14 and B6 was more similar to E18). The analysis revealed that Nude and E14 showed in common the up-regulation of genes associated with tissue remodeling, cytoskeletal rearrangements, wound healing and immune response and the down-regulation of genes coupled to differentiation. Gene expression profiles of regenerative adult Nude mice display features of an attenuated skin development resembling that of E14 mice, thus the Nude mouse may be considered as a unique example of neoteny among mammals. The similar expression profiles of genes in the skin of both Nude and E14 mice are direct or indirect consequences of FOXN1 deficiency. FOXN1 appears to regulate the balance between cell proliferation and differentiation and its lack creates a pro-regenerative environment.

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A FOXN1 mutation competitively displaces wild-type FOXN1 from higher-order nuclear condensates to cause immunodeficiency

Project description:The transcription factor FOXN1 is a master regulator of thymic epithelial cell development and function. Here we demonstrate that FOXN1 expression is differentially regulated during organogenesis and participates in multi-molecular nuclear condensates essential for the factor's transcriptional activity. FOXN1's C-terminal sequence regulates the diffusion velocity within these aggregates and modulates the binding to proximal gene regulatory regions. These dynamics are significantly altered in a patient's FOXN1 mutant modified in its C-terminal sequence. This mutant is transcriptionally inactive and acts as a dominant negative factor displacing wild-type FOXN1 from condensates and causing athymia and severe lymphopenia in heterozygotes. Expression of the mutated mouse ortholog, Foxn1, selectively impairs mouse thymic epithelial cell (TEC) differentiation, revealing a gene dose dependency for individual TEC subtypes. We have therefore identified the cause for a primary immunodeficiency disease and determined the mechanism by which this FOXN1 gain-of-function mutant mediates its dominant negative effect.

2021-10-29 | PXD025552 | Pride

Transcriptional regulation of the thymus master regulator Foxn1 [RNAseq_AR3_vs_nude]

Project description:FOXN1 is a transcription factor critical for the development of both thymic epithelial cell (TEC) and hair follicle cell (HFC) compartments. However, mechanisms controlling its expression remain poorly understood. To address this question, we performed thorough analyses of the conservation and chromatin status of the Foxn1 locus in different tissues and states, and identified several putative cis-regulatory regions unique to TEC vs. HFC. Furthermore, experiments using genetically modified mice with specific deletions in the Foxn1 locus and additional bioinformatic analyses helped us identify key regions and transcription factors involved in either positive or negative regulation of Foxn1 in both TEC and HFC. Specifically, we identified SIX1 and FOXN1 itself, as key factors inducing Foxn1 expression in embryonic and neonatal TECs. Together, our data provide important mechanistic insights into the transcriptional regulation of the Foxn1 gene in TEC vs. HFC and highlight the role of FOXN1 in its autoregulation

2022-08-03 | GSE192872 | GEO

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