Expression of ENL YEATS domain tumor mutations in nephrogenic or stromal lineage impairs kidney development

Recurrent gain-of-function mutations in the histone reader protein ENL have been identified in Wilms tumor, the most prevalent pediatric kidney cancer. However, their pathological significance in kidney development and tumorigenesis in vivo remains elusive. Here, we generate mouse models mimicking E...

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Published inNature communications Vol. 16; no. 1; pp. 2531 - 22
Main Authors Xue, Zhaoyu, Xuan, Hongwen, Lau, Kin, Su, Yangzhou, Wegener, Marc, Li, Kuai, Turner, Lisa, Adams, Marie, Shi, Xiaobing, Wen, Hong
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 14.03.2025
Nature Publishing Group
Nature Portfolio
Subjects
14/19
38/39
38/91
42/41
631/136/2060
631/1647/767/722
631/208/199
631/337/2019
631/67/2332
64/60
82/1
82/51
96/109
96/31
Animal models
Animals
Cell Differentiation - genetics
Cell Lineage - genetics
Epithelium
Female
Forkhead Transcription Factors - genetics
Forkhead Transcription Factors - metabolism
Gene expression
Gene Expression Regulation, Developmental
Glomerulus
Histones
Homeodomain Proteins - genetics
Homeodomain Proteins - metabolism
Humanities and Social Sciences
Humans
Kidney - embryology
Kidney - metabolism
Kidney - pathology
Kidney Neoplasms - genetics
Kidney Neoplasms - pathology
Kidneys
Lethality
Male
Mesenchyme
Mice
multidisciplinary
Mutants
Mutation
Neonates
Organogenesis - genetics
Pediatrics
Science
Science (multidisciplinary)
SIX gene family
Spatial analysis
Stroma
Stromal Cells - metabolism
Stromal Cells - pathology
Transcription Factors - genetics
Transcription Factors - metabolism
Transcriptomics
Tubules
Tumorigenesis
Tumors
Wilms Tumor - genetics
Wilms Tumor - pathology
Wnt protein
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Abstract Recurrent gain-of-function mutations in the histone reader protein ENL have been identified in Wilms tumor, the most prevalent pediatric kidney cancer. However, their pathological significance in kidney development and tumorigenesis in vivo remains elusive. Here, we generate mouse models mimicking ENL tumor (ENL T ) mutations and show that heterozygous mutant expression in Six2 + nephrogenic or Foxd1 + stromal lineages leads to severe, lineage-specific kidney defects, both resulting in neonatal lethality. Six2-ENL T mutant kidneys display compromised cap mesenchyme, scant nephron tubules, and cystic glomeruli, indicative of premature progenitor commitment and blocked differentiation. Bulk and spatial transcriptomic analyses reveal aberrant activation of Hox and Wnt signaling genes in mutant nephrogenic cells. In contrast, Foxd1-ENL T mutant kidneys exhibit expansion in renal capsule and cap mesenchyme, with dysregulated stromal gene expression affecting stroma-epithelium crosstalk. Our findings uncover distinct pathways through which ENL mutations disrupt nephrogenesis, providing a foundation for further investigations into their role in tumorigenesis. The histone reader ENL is frequently mutated in Wilms tumor. Here they use mouse models and spatial transcriptomic analyses to show how ENL tumor mutations disrupt nephrogenesis through distinct pathways in nephrogenic and stromal lineages.
AbstractList Recurrent gain-of-function mutations in the histone reader protein ENL have been identified in Wilms tumor, the most prevalent pediatric kidney cancer. However, their pathological significance in kidney development and tumorigenesis in vivo remains elusive. Here, we generate mouse models mimicking ENL tumor (ENL T ) mutations and show that heterozygous mutant expression in Six2 + nephrogenic or Foxd1 + stromal lineages leads to severe, lineage-specific kidney defects, both resulting in neonatal lethality. Six2-ENL T mutant kidneys display compromised cap mesenchyme, scant nephron tubules, and cystic glomeruli, indicative of premature progenitor commitment and blocked differentiation. Bulk and spatial transcriptomic analyses reveal aberrant activation of Hox and Wnt signaling genes in mutant nephrogenic cells. In contrast, Foxd1-ENL T mutant kidneys exhibit expansion in renal capsule and cap mesenchyme, with dysregulated stromal gene expression affecting stroma-epithelium crosstalk. Our findings uncover distinct pathways through which ENL mutations disrupt nephrogenesis, providing a foundation for further investigations into their role in tumorigenesis. The histone reader ENL is frequently mutated in Wilms tumor. Here they use mouse models and spatial transcriptomic analyses to show how ENL tumor mutations disrupt nephrogenesis through distinct pathways in nephrogenic and stromal lineages.
Recurrent gain-of-function mutations in the histone reader protein ENL have been identified in Wilms tumor, the most prevalent pediatric kidney cancer. However, their pathological significance in kidney development and tumorigenesis in vivo remains elusive. Here, we generate mouse models mimicking ENL tumor (ENLT) mutations and show that heterozygous mutant expression in Six2+ nephrogenic or Foxd1+ stromal lineages leads to severe, lineage-specific kidney defects, both resulting in neonatal lethality. Six2-ENLT mutant kidneys display compromised cap mesenchyme, scant nephron tubules, and cystic glomeruli, indicative of premature progenitor commitment and blocked differentiation. Bulk and spatial transcriptomic analyses reveal aberrant activation of Hox and Wnt signaling genes in mutant nephrogenic cells. In contrast, Foxd1-ENLT mutant kidneys exhibit expansion in renal capsule and cap mesenchyme, with dysregulated stromal gene expression affecting stroma-epithelium crosstalk. Our findings uncover distinct pathways through which ENL mutations disrupt nephrogenesis, providing a foundation for further investigations into their role in tumorigenesis.The histone reader ENL is frequently mutated in Wilms tumor. Here they use mouse models and spatial transcriptomic analyses to show how ENL tumor mutations disrupt nephrogenesis through distinct pathways in nephrogenic and stromal lineages.
Recurrent gain-of-function mutations in the histone reader protein ENL have been identified in Wilms tumor, the most prevalent pediatric kidney cancer. However, their pathological significance in kidney development and tumorigenesis in vivo remains elusive. Here, we generate mouse models mimicking ENL tumor (ENLT) mutations and show that heterozygous mutant expression in Six2+ nephrogenic or Foxd1+ stromal lineages leads to severe, lineage-specific kidney defects, both resulting in neonatal lethality. Six2-ENLT mutant kidneys display compromised cap mesenchyme, scant nephron tubules, and cystic glomeruli, indicative of premature progenitor commitment and blocked differentiation. Bulk and spatial transcriptomic analyses reveal aberrant activation of Hox and Wnt signaling genes in mutant nephrogenic cells. In contrast, Foxd1-ENLT mutant kidneys exhibit expansion in renal capsule and cap mesenchyme, with dysregulated stromal gene expression affecting stroma-epithelium crosstalk. Our findings uncover distinct pathways through which ENL mutations disrupt nephrogenesis, providing a foundation for further investigations into their role in tumorigenesis.Recurrent gain-of-function mutations in the histone reader protein ENL have been identified in Wilms tumor, the most prevalent pediatric kidney cancer. However, their pathological significance in kidney development and tumorigenesis in vivo remains elusive. Here, we generate mouse models mimicking ENL tumor (ENLT) mutations and show that heterozygous mutant expression in Six2+ nephrogenic or Foxd1+ stromal lineages leads to severe, lineage-specific kidney defects, both resulting in neonatal lethality. Six2-ENLT mutant kidneys display compromised cap mesenchyme, scant nephron tubules, and cystic glomeruli, indicative of premature progenitor commitment and blocked differentiation. Bulk and spatial transcriptomic analyses reveal aberrant activation of Hox and Wnt signaling genes in mutant nephrogenic cells. In contrast, Foxd1-ENLT mutant kidneys exhibit expansion in renal capsule and cap mesenchyme, with dysregulated stromal gene expression affecting stroma-epithelium crosstalk. Our findings uncover distinct pathways through which ENL mutations disrupt nephrogenesis, providing a foundation for further investigations into their role in tumorigenesis.
Recurrent gain-of-function mutations in the histone reader protein ENL have been identified in Wilms tumor, the most prevalent pediatric kidney cancer. However, their pathological significance in kidney development and tumorigenesis in vivo remains elusive. Here, we generate mouse models mimicking ENL tumor (ENL ) mutations and show that heterozygous mutant expression in Six2 nephrogenic or Foxd1 stromal lineages leads to severe, lineage-specific kidney defects, both resulting in neonatal lethality. Six2-ENL mutant kidneys display compromised cap mesenchyme, scant nephron tubules, and cystic glomeruli, indicative of premature progenitor commitment and blocked differentiation. Bulk and spatial transcriptomic analyses reveal aberrant activation of Hox and Wnt signaling genes in mutant nephrogenic cells. In contrast, Foxd1-ENL mutant kidneys exhibit expansion in renal capsule and cap mesenchyme, with dysregulated stromal gene expression affecting stroma-epithelium crosstalk. Our findings uncover distinct pathways through which ENL mutations disrupt nephrogenesis, providing a foundation for further investigations into their role in tumorigenesis.
Recurrent gain-of-function mutations in the histone reader protein ENL have been identified in Wilms tumor, the most prevalent pediatric kidney cancer. However, their pathological significance in kidney development and tumorigenesis in vivo remains elusive. Here, we generate mouse models mimicking ENL tumor (ENL T ) mutations and show that heterozygous mutant expression in Six2 + nephrogenic or Foxd1 + stromal lineages leads to severe, lineage-specific kidney defects, both resulting in neonatal lethality. Six2-ENL T mutant kidneys display compromised cap mesenchyme, scant nephron tubules, and cystic glomeruli, indicative of premature progenitor commitment and blocked differentiation. Bulk and spatial transcriptomic analyses reveal aberrant activation of Hox and Wnt signaling genes in mutant nephrogenic cells. In contrast, Foxd1-ENL T mutant kidneys exhibit expansion in renal capsule and cap mesenchyme, with dysregulated stromal gene expression affecting stroma-epithelium crosstalk. Our findings uncover distinct pathways through which ENL mutations disrupt nephrogenesis, providing a foundation for further investigations into their role in tumorigenesis.
Abstract Recurrent gain-of-function mutations in the histone reader protein ENL have been identified in Wilms tumor, the most prevalent pediatric kidney cancer. However, their pathological significance in kidney development and tumorigenesis in vivo remains elusive. Here, we generate mouse models mimicking ENL tumor (ENLT) mutations and show that heterozygous mutant expression in Six2 + nephrogenic or Foxd1 + stromal lineages leads to severe, lineage-specific kidney defects, both resulting in neonatal lethality. Six2-ENLT mutant kidneys display compromised cap mesenchyme, scant nephron tubules, and cystic glomeruli, indicative of premature progenitor commitment and blocked differentiation. Bulk and spatial transcriptomic analyses reveal aberrant activation of Hox and Wnt signaling genes in mutant nephrogenic cells. In contrast, Foxd1-ENLT mutant kidneys exhibit expansion in renal capsule and cap mesenchyme, with dysregulated stromal gene expression affecting stroma-epithelium crosstalk. Our findings uncover distinct pathways through which ENL mutations disrupt nephrogenesis, providing a foundation for further investigations into their role in tumorigenesis.
ArticleNumber 2531
Author Xue, Zhaoyu
Li, Kuai
Shi, Xiaobing
Xuan, Hongwen
Su, Yangzhou
Lau, Kin
Wegener, Marc
Wen, Hong
Adams, Marie
Turner, Lisa
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Snippet Recurrent gain-of-function mutations in the histone reader protein ENL have been identified in Wilms tumor, the most prevalent pediatric kidney cancer....
Abstract Recurrent gain-of-function mutations in the histone reader protein ENL have been identified in Wilms tumor, the most prevalent pediatric kidney...
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631/136/2060
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Animal models
Animals
Cell Differentiation - genetics
Cell Lineage - genetics
Epithelium
Female
Forkhead Transcription Factors - genetics
Forkhead Transcription Factors - metabolism
Gene expression
Gene Expression Regulation, Developmental
Glomerulus
Histones
Homeodomain Proteins - genetics
Homeodomain Proteins - metabolism
Humanities and Social Sciences
Humans
Kidney - embryology
Kidney - metabolism
Kidney - pathology
Kidney Neoplasms - genetics
Kidney Neoplasms - pathology
Kidneys
Lethality
Male
Mesenchyme
Mice
multidisciplinary
Mutants
Mutation
Neonates
Organogenesis - genetics
Pediatrics
Science
Science (multidisciplinary)
SIX gene family
Spatial analysis
Stroma
Stromal Cells - metabolism
Stromal Cells - pathology
Transcription Factors - genetics
Transcription Factors - metabolism
Transcriptomics
Tubules
Tumorigenesis
Tumors
Wilms Tumor - genetics
Wilms Tumor - pathology
Wnt protein
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Title Expression of ENL YEATS domain tumor mutations in nephrogenic or stromal lineage impairs kidney development
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Volume 16
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