Details for: CL0000049

Cell ID: CL0000049

Cell Name: common myeloid progenitor

Description: This cell type is intended to be compatible with any vertebrate common myeloid progenitor. For mammalian CMP known to be CD34-positive, please use the term 'common myeloid progenitor, CD34-positive' (CL_0001059).

Synonyms: common myeloid precursor, CFU-GEMM, CFU-S, CMP, colony forming unit granulocyte, erythrocyte, macrophage, and megakaryocyte, multipotential myeloid stem cell, myeloid stem cell, pluripotent stem cell (bone marrow)

Selected Context(s): Overall

Gene Significance Landscape

Display Options
Score:
Display
Genes

Contexts:

Cell Significance Index (CSI) is uniquely calculated to reveal cell-specific gene markers. More info here

Significant Genes List

Genes with the highest and lowest Percentile Rank Scores (PRS) for common myeloid progenitor within the selected context(s).

Gene ID: A unique numerical identifier for this specific gene.
Symbol: Shortened abbreviation or name that represents this gene.
Ensembl Gene ID: A unique identifier assigned by Ensembl for genomic data mapping.
CSI Score: A combined effect size and statistical significance measure for common myeloid progenitor. Higher scores indicate a stronger, more significant difference in expression.
(Previously described as "Fold Change", but now represents Cliff's Delta × –log10(p).)

Gene ID: A unique numerical identifier for this specific gene.
Symbol: Shortened abbreviation or name that represents this gene.
Ensembl Gene ID: A unique identifier assigned by Ensembl for genomic data mapping.
CSI Score: A combined effect size and statistical significance measure for common myeloid progenitor. Higher scores indicate a stronger, more significant difference in expression.
Average CSI: csi sum / gene count
Cell network configuration

This network visualizes key genes for common myeloid progenitor. It primarily includes:
1. Top genes highly significant for this cell (Num. Top Cell Genes - based on the 'Min. CSI' setting).
2. Any additional specific 'Context Genes' you add below.
The final network is a combined view. Choose an Interaction Source (pathways or protein interactions) and optionally compare CSI scores with a Baseline Cell Type.

Maximum number of selected genes.
Select a context for the baseline cell.
Select a context for the target cell.
Target Cell for CSI:  common myeloid progenitor (CL0000049)

 Legend
Nodes (Genes):
 Query Gene
Node size also reflects Target Cell CSI magnitude.
Node Color (Target Cell CSI in specific network):
 Very High
 High
 Medium
 Low
 Very Low
 N/A or Not Sig.
Edges (Interactions):
 STRING (Protein-Protein)
 ONTOLOGY (Shared Pathway)
 Colors vary by pathway category; default arrow applies.

Loading network (please wait)...

## Summary The [common myeloid progenitor](/details-cell/CL0000049) (CMP) is a multipotent hematopoietic precursor cell responsible for generating all myeloid lineages, including granulocytes, erythrocytes, monocytes, and megakaryocytes. Analysis of its gene significance profile reveals that its identity is defined by a uniquely high and specific expression of genes integral to core cellular machinery. **Overall**, the top markers are not lineage-specific transcription factors but are instead dominated by genes involved in mitochondrial energy production, RNA processing, and protein translation. This suggests that the CMP state is characterized by a high degree of metabolic readiness and biosynthetic potential, maintaining a state of preparedness for rapid differentiation and proliferation upon receiving appropriate lineage-commitment signals. ## Key Characteristics and Function The functional identity of the [common myeloid progenitor](/details-cell/CL0000049) is underscored by the high specificity of genes belonging to several key functional clusters. * **RNA Binding, Splicing, and Stability:** A striking feature of the CMP is the significant expression specificity of a large cohort of heterogeneous nuclear ribonucleoproteins (hnRNPs) and other RNA-binding proteins. This includes [HNRNPA2B1](/details-gene/3181), [HNRNPC](/details-gene/3183), [HNRNPA1](/details-gene/3178), and [HNRNPU](/details-gene/3192), as well as [PABPC1](/details-gene/26986) (Poly(A) Binding Protein) and [YBX1](/details-gene/4904). The high `csi_z` scores for these genes indicate a robust and highly active post-transcriptional regulatory network. This machinery is essential for processing the diverse array of pre-mRNAs required for multi-lineage potential and for rapidly modulating protein expression during differentiation. * **Mitochondrial Respiration and Energy Metabolism:** The CMP is characterized by a strong signature of genes involved in oxidative phosphorylation. Top markers include multiple subunits of the ATP synthase complex ([ATP5MC2](/details-gene/517), [ATP5MG](/details-gene/10632)) and the cytochrome c oxidase complex ([COX4I1](/details-gene/1327), [COX7C](/details-gene/1350)), in addition to the key glycolytic enzyme [GAPDH](/details-gene/2597). This metabolic profile suggests a high energetic state, likely necessary to fuel the demanding processes of cell division and the biosynthesis required for generating large numbers of differentiated progeny. * **Chromatin and Ribosome Biology:** The high specificity of [HMGB1](/details-gene/3146), a non-histone chromosomal protein involved in DNA architecture, and the histone variant [H2AZ1](/details-gene/3015) points to a plastic chromatin environment permissive for widespread gene expression and lineage-specific epigenetic modifications. This is complemented by top markers like [NPM1](/details-gene/4869) and [NCL](/details-gene/4691), which are crucial for ribosome biogenesis, and translation elongation factors ([EEF1B2](/details-gene/1933), [EEF1D](/details-gene/1936)), reinforcing the cell's high capacity for protein synthesis. * **Anti-Markers:** The genes with the lowest expression specificity are not absent but are ubiquitously expressed across many cell types, and thus do not define the CMP state. This list includes components of the antigen presentation pathway ([B2M](/details-gene/567), [HLA E](/details-gene/3133)) and iron storage proteins ([FTH1](/details-gene/2495), [FTL](/details-gene/2512)), functions that are more characteristic of mature, differentiated myeloid cells like macrophages or are generally essential across hematopoietic cells. ## Clinical Significance and Contextual Roles Given that this analysis reflects an **Overall** context, the clinical relevance stems from the fundamental nature of the genes that define the [common myeloid progenitor](/details-cell/CL0000049). Dysregulation of these core processes can have profound consequences, leading to hematological disorders. The high significance of [NPM1](/details-gene/4869) is particularly notable. Mutations in [NPM1](/details-gene/4869) are among the most common genetic alterations in acute myeloid leukemia (AML), a cancer originating from myeloid precursors. This highlights how disruption of a fundamental process like ribosome biogenesis and nucleocytoplasmic transport in a progenitor cell can be a primary driver of malignant transformation. Similarly, [HMGB1](/details-gene/3146), the top marker, is a well-known alarmin or damage-associated molecular pattern (DAMP) that can be released by stressed or dying cells to promote inflammation. Its high intrinsic expression in CMPs suggests these progenitors may be key players in the bone marrow microenvironment, potentially linking hematopoietic stress signals to inflammatory responses. The profile of a cell primed for biosynthesis and proliferation also explains its vulnerability. The cellular machinery that is so specifically expressed in CMPs is often the target of chemotherapeutic agents, which disrupt DNA replication, transcription, and cell division, explaining the profound myelosuppression seen with many cancer treatments. ## Potential Mechanisms and Research Directions 1. **Hypothesis:** The commitment of a [common myeloid progenitor](/details-cell/CL0000049) to a specific lineage (e.g., erythroid vs. granulocytic) is critically regulated at the post-transcriptional level by dynamic changes in the composition of its RNA-binding protein complexes. The highly specific expression of numerous hnRNPs and other RNA-binding proteins like [YBX1](/details-gene/4904) and [PCBP2](/details-gene/5094) suggests they form a regulatory network that controls the stability and translation efficiency of key lineage-determining mRNAs. * **Surprising Findings:** It is notable that a suite of seemingly general RNA processing factors, rather than specific transcription factors, are the most defining markers of this multipotent state. This implies that maintaining multipotency may rely less on the expression of a few master regulators and more on a generalized capacity to rapidly execute any given differentiation program via post-transcriptional control. * **Testable Questions:** Does RIP-seq (RNA immunoprecipitation sequencing) for [HNRNPA1](/details-gene/3178) in CMPs reveal binding to a specific subset of mRNAs, such as those encoding GATA1 or PU.1? Furthermore, does shRNA-mediated knockdown of [HNRNPA1](/details-gene/3178) alter the differentiation outcome of CMPs cultured in multi-lineage-supporting conditions? 2. **Hypothesis:** The bioenergetic state, specifically a reliance on high-efficiency oxidative phosphorylation, is an instructive signal that maintains the multipotency of CMPs. The unique expression signature of mitochondrial components ([ATP5MC2](/details-gene/517), [COX4I1](/details-gene/1327), [UQCRB](/details-gene/7381)) suggests that a high ATP output is not merely permissive but actively suppresses premature differentiation, and that a programmed metabolic shift is a prerequisite for lineage commitment. * **Surprising Findings:** The high specificity (`csi_z`) of core metabolic genes like [GAPDH](/details-gene/2597) and ATP synthase subunits is unexpected for "housekeeping" genes. This suggests that the *quantitative level* of metabolic activity is a critical and unique feature of the CMP state when compared to the broader landscape of cell types. * **Testable Questions:** How does pharmacological inhibition of the electron transport chain (e.g., using rotenone or antimycin A) affect the self-renewal versus differentiation capacity of primary human CMPs in vitro? Does it bias lineage choice, for instance, by favoring less energy-demanding pathways?