Regulation of early T-lineage gene expression and developmental progression by the progenitor cell transcription factor PU.1
Open accessAbstract
The ETS family transcription factor PU.1 is essential for the development of several blood lineages, including T cells, but its function in intrathymic T-cell precursors has been poorly defined. In the thymus, high PU.1 expression persists through multiple cell divisions in early stages but then falls sharply during T-cell lineage commitment. PU.1 silencing is critical for T-cell commitment, but it has remained unknown how PU.1 activities could contribute positively to T-cell development. Here we employed conditional knockout and modified antagonist PU.1 constructs to perturb PU.1 function stage-specifically in early T cells. We show that PU.1 is needed for full proliferation, restricting access to some non-T fates, and controlling the timing of T-cell developmental progression such that removal or antagonism of endogenous PU.1 allows precocious access to T-cell differentiation. Dominant-negative effects reveal that this repression by PU.1 is mediated indirectly. Genome-wide transcriptome analysis identifies novel targets of PU.1 positive and negative regulation affecting progenitor cell signaling and cell biology and indicating distinct regulatory effects on different subsets of progenitor cell transcription factors. Thus, in addition to supporting early T-cell proliferation, PU.1 regulates the timing of activation of the core T-lineage developmental program.
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PU.1 represses cell cycle genes in T cell progenitors.
“PU.1 similarly represses cell cycle genes in T cell progenitors”
From PU.1 is required to restrain myelopoiesis during chronic inflammatory stress (2023) · cites this paper as Champhekar et al., 2015
The Results section on DN progression reports that PU.1-deficient DN2 cells proliferated significantly less than controls; PU.1 was needed for optimal proliferation. The genome-wide Results section also says the PU.1 repressor construct had little, if any, impact on major cell-cycle regulators. These passages do not support the claim that PU.1 represses cell-cycle genes in T-cell progenitors. (LLM, conf=0.88)
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredPU.1-deficient cells underwent fewer cycles per unit time than controls in ETP and DN2a/2b stages.
“PU.1-deficient cells underwent fewer cycles per unit time than controls both in ETP stage and in DN2a/2b stages (79)”
From Mechanisms of Action of Hematopoietic Transcription Factor PU.1 in Initiation of T-Cell Development (2019) · cites this paper as [79]
The Results section (‘PU.1 is required for DN progression and survival’) reports significantly less proliferation in PU.1-knockout DN2 cells than in controls after two and three days. It also describes less overall proliferation after deletion at ETP or DN2a, but does not establish fewer cell cycles specifically in ETP cells or separately in DN2b cells. (LLM, conf=0.84)
Experimental — accuracy not yet measuredPU.1 can upregulate progenitor-associated genes Bcl11a, Lmo2, Mef2c, and Hhex above their normal levels in DN2a and DN2b primary cells, whereas PU.1-ENG can downregulate them.
“whereas PU.1 itself can upregulate progenitor-associated genes Bcl11a, Lmo2, Mef2c, and Hhex above their normal levels in DN2a and DN2b primary cells, PU.1-ENG can downregulate them (79).”
From Mechanisms of Action of Hematopoietic Transcription Factor PU.1 in Initiation of T-Cell Development (2019) · cites this paper as [79]
In Results, under “Selective roles for PU.1 in the progenitor-associated regulatory gene network” (page unavailable), the paper reports that added wild-type PU.1 up-regulated Bcl11a, Lmo2, and Mef2c, consistent with effects of PU.1-Eng. It does not name Hhex among those genes, so the claim about all four is not fully supported by our copy. (LLM, conf=0.86)
Experimental — accuracy not yet measuredPU.1-ENG has some spurious effects and cannot access closed chromatin sites as well as full-length PU.1.
“However, PU.1-ENG also has some spurious effects and cannot access closed chromatin sites as well as full-length PU.1 (79, 85).”
From Mechanisms of Action of Hematopoietic Transcription Factor PU.1 in Initiation of T-Cell Development (2019) · cites this paper as [79]
The Discussion (page unavailable) acknowledges caveats of forced PU.1-Eng expression and reports that some genes bound by endogenous PU.1 were unaffected by PU.1-Eng. The Results section on specificity (page unavailable) tests for side effects but finds the construct selective. Neither passage establishes that PU.1-Eng has spurious effects or that its weaker response at some sites is due to an inability to access closed chromatin relative to full-length PU.1. (LLM, conf=0.82)
Experimental — accuracy not yet measuredCells remaining within the T-cell pathway, continuing CD25 and negative CD11b, show relatively modest and selective changes in gene expression driven by upregulated PU.1, with minimal loss of T-cell regulatory gene expression.
“In contrast, cells remaining within the T-cell pathway, continuing to express CD25 and remaining negative for CD11b, show relatively modest and selective changes in gene expression driven by upregulated PU.1, with minimal loss of T-cell regulatory gene expression (79, 85).”
From Mechanisms of Action of Hematopoietic Transcription Factor PU.1 in Initiation of T-Cell Development (2019) · cites this paper as [79]
The Results section on PU.1-Eng specificity identifies CD25 expression and absence of CD11b as markers of cells not diverted to a myeloid fate. But the Results section on negative regulation of T-cell development reports that overexpressed wild-type PU.1 down-regulated multiple T-lineage genes, including Tcf7, Gata3, Lef1, and Ikaros, with effects much greater than those of PU.1 deletion. Our copy does not establish that the CD25-positive, CD11b-negative cells specifically had modest expression changes or minimal loss of T-cell regulatory gene expression (page numbers unavailable). (LLM, conf=0.82)
Experimental — accuracy not yet measured
The PU.1-ENG obligate repressor should affect PU.1 positive regulation targets in the opposite direction from wildtype PU.1, and in theory should affect PU.1 negative regulation targets in the same direction.
“The obligate repressor should affect PU.1 positive regulation targets in the opposite direction from wildtype PU.1, and in theory should affect PU.1 negative regulation targets in the same direction, an “algebraic sign” distinction that could be used in principle to dissect indirect effects as well (79).”
From Mechanisms of Action of Hematopoietic Transcription Factor PU.1 in Initiation of T-Cell Development (2019) · cites this paper as [79]
The Results section describes PU.1-Eng as an obligate repressor that antagonizes PU.1-dependent activation, supporting the predicted opposite effect on positively regulated targets. In “Negative regulation of T-cell development by PU.1 is indirect” (page unavailable), it predicts the same effect as wild-type PU.1 only for directly repressed genes; genes repressed indirectly through an intermediate repressor would instead be up-regulated by PU.1-Eng. (LLM, conf=0.86)
Experimental — accuracy not yet measuredIn pro-T cells, the genes that are repressed when exogenous PU.1 is introduced are not necessarily linked to the sites that the exogenous PU.1 actually binds.
“However, in the pro-T cells, the genes that are repressed when exogenous PU.1 is introduced are not necessarily linked to the sites that the exogenous PU.1 actually binds.”
From Mechanisms of Action of Hematopoietic Transcription Factor PU.1 in Initiation of T-Cell Development (2019) · cites this paper as [79]
The Results section on PU.1-Eng and endogenous PU.1 binding reports that repressed genes were enriched for associated PU.1-binding sites, though those sites were sometimes intronic or flanking rather than at promoters. The cited analysis measures endogenous PU.1 occupancy, not where the introduced PU.1-Eng actually binds, so it does not establish the claim about exogenous binding sites. (LLM, conf=0.78)
Experimental — accuracy not yet measuredPU.1 is not uniquely responsible for the Phase 1 gene expression pattern; other Phase 1 genes are either unaffected or moderately inhibited by PU.1.
“PU.1 is not uniquely responsible for the Phase 1 gene expression pattern, however, for other Phase 1 genes are either unaffected or moderately inhibited by PU.1, as discussed elsewhere (79, 123).”
From Mechanisms of Action of Hematopoietic Transcription Factor PU.1 in Initiation of T-Cell Development (2019) · cites this paper as [79]
The Discussion (page unavailable) rules out PU.1 as a global positive regulator of Phase 1 genes and says it blunts expression of one group. The Results section on the progenitor-associated regulatory gene network (page unavailable) likewise reports repression of several Phase 1 genes, but the cited passages do not establish that other Phase 1 genes are unaffected or that the inhibition is moderate. (LLM, conf=0.82)
Experimental — accuracy not yet measuredPU.1 provides positive input into a discrete subset of Phase 1 regulatory genes, with Mef2c, Lmo2, Bcl11a, and often also Hhex responding over a range of different tests.
“Varied PU.1 gain and loss of function perturbations in the DN2-DN3 stages show that PU.1 does provide positive input into a discrete subset of Phase 1 regulatory genes, with Mef2c, Lmo2, Bcl11a, and often also Hhex responding over a range of different tests (58, 79, 80, 85).”
From Mechanisms of Action of Hematopoietic Transcription Factor PU.1 in Initiation of T-Cell Development (2019) · cites this paper as [79]
The Results section on selective roles for PU.1 reports that added PU.1 up-regulated Bcl11a, Lmo2, and Mef2c, consistent with deletion and PU.1-Eng tests; the Discussion identifies them as a subset of phase 1 genes positively regulated by PU.1. The passages do not establish the claimed response of Hhex, and the reported deletion effects concern DN1 and early DN2 cells rather than DN2–DN3 stages throughout. No page numbers are available in our copy. (LLM, conf=0.88)
Experimental — accuracy not yet measuredPro-T cells that have PU.1 acutely deleted at an early stage differentiate faster along the T lineage and tend to shift to a natural killer-like program more readily than controls.
“Indeed, pro-T cells that have PU.1 acutely deleted at an early stage do not only differentiate faster along the T lineage; they also tend to shift to a natural killer-like program more readily than controls (79).”
From Mechanisms of Action of Hematopoietic Transcription Factor PU.1 in Initiation of T-Cell Development (2019) · cites this paper as [79]
The Results section reports that deleting PU.1 at the ETP or DN2a stage made early T cells differentiate faster than controls. It also reports greater NK-cell production under permissive conditions, but that result concerns progeny of PU.1-deficient fetal liver precursors, not the same early-stage pro-T cells. The claim conflates those populations and omits the NK-development condition. (LLM, conf=0.88)
Experimental — accuracy not yet measuredCell cycle restriction may play a similar role in lymphoid development.
“and thus cell cycle restriction may play a similar role in lymphoid development (Kueh et al., 2013; Staber et al., 2013; Champhekar et al., 2015).”
From PU.1 is required to restrain myelopoiesis during chronic inflammatory stress (2023) · cites this paper as Champhekar et al., 2015
The Results (page unavailable) show that PU.1-deficient early T cells proliferated less yet differentiated faster, supporting a possible link between reduced proliferation and lymphoid development. The paper does not establish that cell-cycle restriction itself drives that progression; both changes followed PU.1 deletion. (LLM, conf=0.82)
Experimental — accuracy not yet measuredA substantially larger fraction of cells generated from PU.1-disrupted precursors progressed to DN3 than controls over the same absolute developmental time.
“of the cells that were generated from PU.1-disrupted precursors, a substantially larger fraction progressed to DN3 stage than in control cells, over the same length of absolute developmental time, suggesting that they were liberated from a differentiation constraint (79, 80).”
From Mechanisms of Action of Hematopoietic Transcription Factor PU.1 in Initiation of T-Cell Development (2019) · cites this paper as [79]
PU.1 is important within the T-cell program as well as before thymic entry.
“PU.1 is indeed important within the T-cell program as well as before thymic entry, as shown by using in vitro differentiation to provide conditions where PU.1 could be removed acutely in a synchronized cohort of precursors and the fates of the cells could be monitored immediately afterwards.”
From Mechanisms of Action of Hematopoietic Transcription Factor PU.1 in Initiation of T-Cell Development (2019) · cites this paper as [79]
In both experimental setups, PU.1 disruption reduced T-cell precursor proliferation substantially compared to controls.
“In both experimental setups, PU.1 disruption reduced T-cell precursor proliferation substantially as compared to controls.”
From Mechanisms of Action of Hematopoietic Transcription Factor PU.1 in Initiation of T-Cell Development (2019) · cites this paper as [79]
Effects on target gene regulation appear very weak at timepoints up to 2 days after PU.1 deletion, despite reduced cell yields from knockout cells showing that PU.1 is biologically important.
“the effects on target gene regulation appear very weak at timepoints up to 2 days after PU.1 deletion, despite the fact that the reduced cell yields from the knockout cells show that PU.1 is biologically important (79).”
From Mechanisms of Action of Hematopoietic Transcription Factor PU.1 in Initiation of T-Cell Development (2019) · cites this paper as [79]
The developmental speed-up observed in primary pro-T cells when PU.1 is knocked out points to a normal PU.1 role as a brake on developmental progression.
“it is important to note that the developmental speed-up observed in primary pro-T cells when PU.1 is knocked out also points to a normal PU.1 role as a brake on developmental progression (79).”
From Mechanisms of Action of Hematopoietic Transcription Factor PU.1 in Initiation of T-Cell Development (2019) · cites this paper as [79]
The PU.1-ENG obligate repressor downregulated genes that are positive regulatory targets of wildtype PU.1, but upregulated many genes that wildtype PU.1 represses, inconsistent with a direct repression mechanism.
“while the obligate repressor downregulated genes that are positive regulatory targets of wildtype PU.1, it actually upregulated many genes that wildtype PU.1 represses, completely inconsistent with a direct repression mechanism (79).”
From Mechanisms of Action of Hematopoietic Transcription Factor PU.1 in Initiation of T-Cell Development (2019) · cites this paper as [79]
Even with PU.1 transduction, Scid.adh.2C2 cells do not restore the full chromatin accessibility landscape of ETP and DN2a pro-T cells and reactivate little of the normal context program.
“Even with PU.1 transduction, Scid.adh.2C2 cells do not restore the full chromatin accessibility landscape of ETP and DN2a stage pro-T cells, and despite detectable upregulation of a few other early pro-T cell genes (e.g., Bcl11a and Lyl1), the transduced cells as a whole reactivate little of the program that forms the normal context for endogenous PU.1 activity in pro-T cells (58, 79, 85).”
From Mechanisms of Action of Hematopoietic Transcription Factor PU.1 in Initiation of T-Cell Development (2019) · cites this paper as [79]
The Results section on PU.1-Eng specificity reports that wild-type PU.1 transduction of Adh.2C2 cells causes myeloid diversion and represses many T-cell genes. It does not assess whether those cells restore ETP/DN2a chromatin accessibility or how much of the early pro-T-cell program they reactivate. Searches for chromatin accessibility and early-program reactivation in Adh.2C2 cells did not find a passage establishing either point. (LLM, conf=0.73)
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Self-citationSpi-1/PU.1 activates transcription through clustered DNA occupancy in erythroleukemia
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The cis-Regulatory Atlas of the Mouse Immune System
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Self-citationHow transcription factors drive choice of the T cell fate
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Self-citationAsynchronous combinatorial action of four regulatory factors activates Bcl11b for T cell commitment
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Self-citationRecurrent SPI1 (PU.1) fusions in high-risk pediatric T cell acute lymphoblastic leukemia
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Self-citationEnvironmental sensing by mature B cells is controlled by the transcription factors PU.1 and SpiB
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Self-citationBcl11b sets pro-T cell fate by site-specific cofactor recruitment and by repressing Id2 and Zbtb16
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Self-citationMechanisms of Action of Hematopoietic Transcription Factor PU.1 in Initiation of T-Cell Development
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Self-citationTranscription factor PU.1 and immune cell differentiation (Review)
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Bcl11b and combinatorial resolution of cell fate in the T-cell gene regulatory network
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Self-citationCytokines, Transcription Factors, and the Initiation of T-Cell DevelopmentPreprint
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Self-citationUngerbäck, J., Hosokawa, H., Wang, X., Strid, T., Williams, B. A., Sigvardsson, M., & Rothenberg, E. V. (2018) · Genome Research · doi:10.1101/gr.231423.117 · Cited by 77 · see citing works
Self-citationProgramming for T-lymphocyte fates: modularity and mechanismsPreprint
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Self-citation2014 Jeffrey M. Hoeg Award Lecture
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Cell type–specific actions of Bcl11b in early T-lineage and group 2 innate lymphoid cells
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Self-citationMolecular regulation of peripheral B cells and their progeny in immunityPreprint
Boothby, M. R., Hodges, E. C., & Thomas, J. W. (2019) · Genes & Development · doi:10.1101/gad.320192.118 · Cited by 65 · see citing works
Rothenberg, E. V., Ungerbäck, J., & Champhekar, A. (2016) · Advances in Immunology · doi:10.1016/bs.ai.2015.09.002 · Cited by 61 · see citing works
Self-citationLin, Y., Zhang, Q., Zhang, H., Liu, W., Liu, C., Li, Q., & Guo, A. (2015) · Scientific Reports · doi:10.1038/srep15215 · Cited by 57 · see citing works
Zhou, W., Gao, F., Romero-Wolf, M., Jo, S., & Rothenberg, E. V. (2022) · Science Immunology · doi:10.1126/sciimmunol.abm1920 · Cited by 56 · see citing works
Self-citationDai, Y.-T., Zhang, F., Fang, H., Li, J.-F., Lu, G., Jiang, L., Chen, B., Mao, D.-D., Liu, Y.-F., Wang, J., et al. (2022) · Proceedings of the National Academy of Sciences of the United States of America · doi:10.1073/pnas.2120787119 · Cited by 50 · see citing works
Shin, B., Hosokawa, H., Romero-Wolf, M., Zhou, W., Masuhara, K., Tobin, V. R., Levanon, D., Groner, Y., & Rothenberg, E. V. (2021) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2019655118 · Cited by 53 · see citing works
Self-citationOBF1 and Oct factors control the germinal center transcriptional program
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Self-citationWang, S.-F., He, Q.-P., Ma, D.-Y., Xue, Y.-F., & Liu, F. (2015) · Developmental Cell · doi:10.1016/j.devcel.2015.07.011 · Cited by 34 · see citing works
Hematopoiesis and T‐cell specification as a model developmental system
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Self-citationT-ALL leukemia stem cell 'stemness' is epigenetically controlled by the master regulator SPI1
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Hematopoietic stem cell lineage specification
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Transcriptional network dynamics in early T cell development
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Stage-specific action of Runx1 and GATA3 controls silencing of PU.1 expression in mouse pro–T cells
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Self-citationLogic and lineage impacts on functional transcription factor deployment for T-cell fate commitment
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Self-citationMapping the landscape of chromatin dynamics during naïve CD4+ T-cell activation
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Dynamic control of the T-cell specification gene regulatory network
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Self-citationPU.1 is required to restrain myelopoiesis during chronic inflammatory stress
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“1 similarly represses cell cycle genes in T cell progenitors, and thus cell cycle restriction may play a similar role in lymphoid development (Kueh et al., 2013; Staber et al., 2013; Champhekar et al., 2015).”
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- Authors
- Champhekar, A., Damle, S. S., Freedman, G., Carotta, S., Nutt, S. L., & Rothenberg, E. V.
- Affiliations
- California Institute of Technology (US)
- The University of Melbourne (AU)
- Corresponding author
- Rothenberg, Ellen V.
- Venue
- Genes & Development
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2015-04-06
- Volume
- 29
- Issue
- 8
- Pages
- 832-848
- ISSN
- 0890-9369 (ISSN-L)
- 1549-5477
- PMC
- PMC4403259
- OpenAlex
- W2098219736
- Cited by
- 74
- References
- 53
- Citations by year
- 2026: 4 · 2025: 4 · 2024: 4 · 2023: 4 · 2022: 4 · 2021: 11 · 2020: 5 · 2019: 8 · 2018: 11 · 2017: 7 · 2016: 8 · 2015: 4
- Type
- posted content
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by-nc
- Locations
- Genes & Development (publishedVersion, cc-by-nc)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- CaltechAUTHORS (California Institute of Technology) (submittedVersion, cc-by-nc)
- Funders
- National Institutes of Health (CA90233, AI95943, HD076915)
- Louis A. Garfinkle Memorial Laboratory Fund
- Al Sherman Foundation
- Albert Billings Ruddock Professorship
- Victorian State Government Operational Infrastructure Support
- National Health and Medical Research Council of Australia Independent Research Institute Infrastructure Support (361646, 105492, 1058238)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Keywords
- PU.1, ETS transcription factors, T cell development, T cell lineage commitment, T cell proliferation, conditional knockout, genome-wide transcriptome, transcriptional regulation
- MeSH terms
- Proto-Oncogene Protein Spi-1, Animals, Cell Differentiation, Cell Survival, Cells, Cultured, Mice, Inbred C57BL, Proto-Oncogene Proteins, Stem Cells, T-Lymphocytes, Trans-Activators, Gene Expression Regulation, Developmental, Receptors, Notch, Transcriptome
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