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Impaired In Vitro Erythropoiesis following Deletion of the Scl ( Tal1 ) +40 Enhancer Is Largely Compensated for In Vivo despite a Significant Reduction in Expression
Abstract
The Scl (Tal1) gene encodes a helix-loop-helix transcription factor essential for hematopoietic stem cell and erythroid development. The Scl +40 enhancer is situated downstream of Map17, the 3' flanking gene of Scl, and is active in transgenic mice during primitive and definitive erythropoiesis. To analyze the in vivo function of the Scl +40 enhancer within the Scl/Map17 transcriptional domain, we deleted this element in the germ line. Scl(Δ40/Δ40) mice were viable with reduced numbers of erythroid CFU in both bone marrow and spleen yet displayed a normal response to stress hematopoiesis. Analysis of Scl(Δ40/Δ40) embryonic stem (ES) cells revealed impaired erythroid differentiation, which was accompanied by a failure to upregulate Scl when erythropoiesis was initiated. Map17 expression was also reduced in hematopoietic tissues and differentiating ES cells, and the Scl +40 element was able to enhance activity of the Map17 promoter. However, only Scl but not Map17 could rescue the Scl(Δ40/Δ40) ES phenotype. Together, these data demonstrate that the Scl +40 enhancer is an erythroid cell-specific enhancer that regulates the expression of both Scl and Map17. Moreover, deletion of the +40 enhancer causes a novel erythroid phenotype, which can be rescued by ectopic expression of Scl but not Map17.
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“The top 10 TF binding sites with the highest methylation increase in Tet2-KO relative to WT upon IL1β stimulation in CMPs included GATA1, TAL1, and MAZ which promote erythropoiesis (Fig. 4c)35–37.”
From Clonal hematopoiesis related TET2 loss-of-function impedes IL1β-mediated epigenetic reprogramming in hematopoietic stem and progenitor cells (2023) · cites this paper as [35]
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Cites
Absence of blood formation in mice lacking the T-cell leukaemia oncoprotein tal-1/SCL
Shivdasani, R. A., Mayer, E. L., & Orkin, S. H. (1995) · Nature · doi:10.1038/373432a0 · Cited by 938
Phenotypic robustness conferred by apparently redundant transcriptional enhancers
Frankel, N., Davis, G. K., Vargas, D., Wang, S., Payre, F., & Stern, D. L. (2010) · Nature · doi:10.1038/nature09158 · Cited by 510
Mikkola, H. K. A., Klintman, J., Yang, H., Hock, H., Schlaeger, T. M., Fujiwara, Y., & Orkin, S. H. (2003) · Nature · doi:10.1038/nature01345 · Cited by 371
Reactivation of hepatic EPO synthesis in mice after PHD loss
Minamishima, Y. A., & Kaelin, W. G. (2010) · Science · doi:10.1126/science.1192811 · Cited by 163
Molecular Signatures of Quiescent, Mobilized and Leukemia-Initiating Hematopoietic Stem Cells
Forsberg, E. C., Passegué, E., Prohaska, S. S., Wagers, A. J., Koeva, M., Stuart, J. M., & Weissman, I. L. (2010) · PLoS ONE · doi:10.1371/journal.pone.0008785 · Cited by 127
Bender, M. A., Byron, R., Ragoczy, T., Telling, A., Bulger, M., & Groudine, M. (2006) · Blood · doi:10.1182/blood-2006-04-014431 · Cited by 59
Research works printed but not linked: 53
- 10.1016/S0092-8674(00)80076-8 · DOI
- 10.1002/j.1460-2075.1996.tb00787.x · DOI
- 10.1073/pnas.92.15.7075 · DOI · Paper page
- 10.1101/gad.12.4.473 · DOI
- 10.1111/j.1460-9568.2006.04712.x · DOI
- 10.1182/blood.V94.11.3754 · DOI
- 10.1016/S0306-4522(03)00571-2 · DOI · Paper page
- Green AR, Lints T, Visvader J, Harvey R, Begley CG. 1992. SCL is coexpressed with GATA-1 in hemopoietic cells but is also expressed in developing brain. Oncogene 7:653–660.
- Visvader J, Begley CG, Adams JM. 1991. Differential expression of the LYL, SCL and E2A helix-loop-helix genes within the hemopoietic system. Oncogene 6:187–194.
- 10.1038/nature07679 · DOI
- 10.1182/blood-2003-09-3202 · DOI
- 10.1073/pnas.0237324100 · DOI
- 10.1182/blood-2006-10-053124 · DOI
- 10.1128/MCB.25.15.6355-6362.2005 · DOI
- 10.1128/MCB.25.12.5215-5225.2005 · DOI
- 10.1128/MCB.00870-10 · DOI
- Kocher O, Cheresh P, Brown LF, Lee SW. 1995. Identification of a novel gene, selectively up-regulated in human carcinomas, using the differential display technique. Clin. Cancer Res. 1:1209–1215.
- 10.1046/j.1523-1747.2000.00071.x · DOI
- 10.1371/journal.pgen.0010028 · DOI
- 10.1152/physiolgenomics.00247.2006 · DOI
- 10.1093/carcin/bgm083 · DOI
- 10.1016/j.devcel.2011.04.008 · DOI
- 10.1128/MCB.24.5.1870-1883.2004 · DOI
- 10.1093/emboj/cdf286 · DOI · Paper page
- 10.1128/MCB.00931-07 · DOI
- 10.1006/dbio.1999.9236 · DOI
- 10.1634/stemcells.2005-0090 · DOI
- 10.1101/gr.749203 · DOI
- 10.1002/gene.10043 · DOI
- 10.1182/blood-2009-02-206573 · DOI
- 10.1242/dev.01044 · DOI
- 10.1074/jbc.273.44.29032 · DOI
- 10.1016/j.exphem.2007.05.011 · DOI
- 10.1016/j.exphem.2012.02.006 · DOI
- 10.1182/blood-2007-12-128900 · DOI
- 10.1182/blood-2006-03-013656 · DOI · Paper page
- 10.1182/blood-2006-05-023226 · DOI
- 10.1002/j.1460-2075.1992.tb05500.x · DOI
- 10.1073/pnas.101532998 · DOI
- 10.1074/jbc.272.13.8781 · DOI
- 10.1182/blood.V86.4.1502.bloodjournal8641502 · DOI
- 10.1101/gr.1759004 · DOI
- 10.1182/blood-2004-08-3037 · DOI · Paper page
- 10.1038/72635 · DOI
- 10.1038/sj.onc.1201426 · DOI
- 10.1242/dev.126.17.3891 · DOI
- 10.1242/dev.00149 · DOI
- 10.1182/blood-2004-04-1247 · DOI
- 10.1182/blood-2009-01-201384 · DOI
- 10.1002/bies.201100121 · DOI · Paper page
- 10.1371/journal.pbio.0050234 · DOI
- 10.1182/blood-2002-05-1409 · DOI · Paper page
- 10.1182/blood-2010-10-313031 · DOI
Cited by
Hughes, J. R., Roberts, N., McGowan, S., Hay, D., Giannoulatou, E., Lynch, M., De Gobbi, M., Taylor, S., Gibbons, R., & Higgs, D. R. (2014) · Nature Genetics · doi:10.1038/ng.2871 · Cited by 461
The pluripotent regulatory circuitry connecting promoters to their long-range interacting elements
Schoenfelder, S., Furlan-Magaril, M., Mifsud, B., Tavares-Cadete, F., Sugar, R., Javierre, B.-M., Nagano, T., Katsman, Y., Sakthidevi, M., Wingett, S. W., et al. (2015) · Genome Research · doi:10.1101/gr.185272.114 · Cited by 460
Self-citationMcClatchy, J., Strogantsev, R., Wolfe, E., Lin, H. Y., Mohammadhosseini, M., Davis, B. A., Eden, C., Goldman, D., Fleming, W. H., Conley, P., et al. (2023) · Nature Communications · doi:10.1038/s41467-023-43697-y · Cited by 95
Metadata
- Authors
- Ferreira, R., Spensberger, D., Silber, Y., Dimond, A., Li, J., Green, A. R., & Göttgens, B.
- Venue
- Molecular and Cellular Biology
- Publisher
- Informa UK Limited
- Published
- 2013-03-01
- Volume
- 33
- Issue
- 6
- Pages
- 1254-1266
- ISSN
- 1098-5549
- Cited by
- 12
- References
- 6
- Language
- en
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- CoChat. (2026). Citation check: Impaired In Vitro Erythropoiesis following Deletion of the Scl ( Tal1 ) +40 Enhancer Is Largely Compensated for In Vivo despite a Significant Reduction in Expression. https://app.cochat.ai/papers/10.1128/mcb.01525-12
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- Ferreira, R., Spensberger, D., Silber, Y., Dimond, A., Li, J., Green, A. R., & Göttgens, B. (2013). Impaired In Vitro Erythropoiesis following Deletion of the Scl ( Tal1 ) +40 Enhancer Is Largely Compensated for In Vivo despite a Significant Reduction in Expression. Molecular and Cellular Biology. https://doi.org/10.1128/mcb.01525-12
