NKL Homeobox Gene VENTX Is Part of a Regulatory Network in Human Conventional Dendritic Cells.
Stefan NagelClaudia PommerenkeCorinna MeyerHans Günther DrexlerPublished in: International journal of molecular sciences (2021)
Recently, we documented a hematopoietic NKL-code mapping physiological expression patterns of NKL homeobox genes in human myelopoiesis including monocytes and their derived dendritic cells (DCs). Here, we enlarge this map to include normal NKL homeobox gene expressions in progenitor-derived DCs. Analysis of public gene expression profiling and RNA-seq datasets containing plasmacytoid and conventional dendritic cells (pDC and cDC) demonstrated HHEX activity in both entities while cDCs additionally expressed VENTX. The consequent aim of our study was to examine regulation and function of VENTX in DCs. We compared profiling data of VENTX-positive cDC and monocytes with VENTX-negative pDC and common myeloid progenitor entities and revealed several differentially expressed genes encoding transcription factors and pathway components, representing potential VENTX regulators. Screening of RNA-seq data for 100 leukemia/lymphoma cell lines identified prominent VENTX expression in an acute myelomonocytic leukemia cell line, MUTZ-3 containing inv(3)(q21q26) and t(12;22)(p13;q11) and representing a model for DC differentiation studies. Furthermore, extended gene analyses indicated that MUTZ-3 is associated with the subtype cDC2. In addition to analysis of public chromatin immune-precipitation data, subsequent knockdown experiments and modulations of signaling pathways in MUTZ-3 and control cell lines confirmed identified candidate transcription factors CEBPB, ETV6, EVI1, GATA2, IRF2, MN1, SPIB, and SPI1 and the CSF-, NOTCH-, and TNFa-pathways as VENTX regulators. Live-cell imaging analyses of MUTZ-3 cells treated for VENTX knockdown excluded impacts on apoptosis or induced alteration of differentiation-associated cell morphology. In contrast, target gene analysis performed by expression profiling of knockdown-treated MUTZ-3 cells revealed VENTX-mediated activation of several cDC-specific genes including CSFR1, EGR2, and MIR10A and inhibition of pDC-specific genes like RUNX2. Taken together, we added NKL homeobox gene activities for progenitor-derived DCs to the NKL-code, showing that VENTX is expressed in cDCs but not in pDCs and forms part of a cDC-specific gene regulatory network operating in DC differentiation and function.
Keyphrases
- dendritic cells
- genome wide identification
- transcription factor
- genome wide
- rna seq
- single cell
- immune response
- regulatory t cells
- copy number
- dna methylation
- dna binding
- healthcare
- endothelial cells
- cell cycle
- induced apoptosis
- genome wide analysis
- electronic health record
- cell proliferation
- liver failure
- poor prognosis
- mental health
- acute myeloid leukemia
- acute lymphoblastic leukemia
- bone marrow
- binding protein
- emergency department
- data analysis
- high glucose
- long non coding rna
- intensive care unit
- machine learning
- mass spectrometry
- magnetic resonance imaging
- gene expression
- signaling pathway
- drug induced
- big data
- stem cells
- artificial intelligence
- pi k akt
- dna damage
- mesenchymal stem cells
- induced pluripotent stem cells
- fluorescence imaging