Molecular Mechanisms of Lupus Susceptibility Allele PBX1D
Pre–B cell leukemia homeobox 1 (PBX1) controls chromatin accessibility to a large number of genes in various cell types. Its dominant negative splice isoform, PBX1D, which lacks the DNA and Hox-binding domains, is expressed more frequently in the CD4+ T cells from lupus-prone mice and patients with...
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| Published in | The Journal of immunology (1950) Vol. 211; no. 5; pp. 727 - 734 |
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| Main Authors | , , , , , , , |
| Format | Journal Article |
| Language | English |
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United States
01.09.2023
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| Abstract | Pre–B cell leukemia homeobox 1 (PBX1) controls chromatin accessibility to a large number of genes in various cell types. Its dominant negative splice isoform, PBX1D, which lacks the DNA and Hox-binding domains, is expressed more frequently in the CD4+ T cells from lupus-prone mice and patients with systemic lupus erythematosus than healthy control subjects. PBX1D overexpression in CD4+ T cells impaired regulatory T cell homeostasis and expanded inflammatory CD4+ T cells. In this study, we showed that PBX1 message expression is downregulated by activation in CD4+ T cells as well as in B cells. PBX1D protein was less stable than the normal isoform, PBX1B, and it is degraded through the ubiquitin-proteasome–dependent pathway. The DNA binding domain lacking in PBX1D has two putative ubiquitin binding sites, K292 and K293, that are predicted to be in direct contact with DNA. Mutation of K292-293 reduced PBX1B stability to a level similar to PBX1D and abrogated DNA binding. In addition, contrary to PBX1B, PBX1D is retained in the cytoplasm without the help of the cofactors MEIS or PREP1, indicating a different requirement for nuclear translocation. Overall, these findings suggest that multiple post-transcriptional mechanisms are responsible for PBX1D loss of function and induction of CD4+ T cell inflammatory phenotypes in systemic lupus erythematosus. |
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| AbstractList | Pre–B cell leukemia homeobox 1 (PBX1) controls chromatin accessibility to a large number of genes in various cell types. Its dominant negative splice isoform, PBX1D, which lacks the DNA and Hox-binding domains, is expressed more frequently in the CD4+ T cells from lupus-prone mice and patients with systemic lupus erythematosus than healthy control subjects. PBX1D overexpression in CD4+ T cells impaired regulatory T cell homeostasis and expanded inflammatory CD4+ T cells. In this study, we showed that PBX1 message expression is downregulated by activation in CD4+ T cells as well as in B cells. PBX1D protein was less stable than the normal isoform, PBX1B, and it is degraded through the ubiquitin-proteasome–dependent pathway. The DNA binding domain lacking in PBX1D has two putative ubiquitin binding sites, K292 and K293, that are predicted to be in direct contact with DNA. Mutation of K292-293 reduced PBX1B stability to a level similar to PBX1D and abrogated DNA binding. In addition, contrary to PBX1B, PBX1D is retained in the cytoplasm without the help of the cofactors MEIS or PREP1, indicating a different requirement for nuclear translocation. Overall, these findings suggest that multiple post-transcriptional mechanisms are responsible for PBX1D loss of function and induction of CD4+ T cell inflammatory phenotypes in systemic lupus erythematosus. Pre-B cell leukemia homeobox 1 (PBX1) controls chromatin accessibility to a large number of genes in various cell types. Its dominant negative splice isoform, PBX1D, which lacks the DNA and Hox-binding domains, is expressed more frequently in the CD4+ T cells from lupus-prone mice and patients with systemic lupus erythematosus than healthy control subjects. PBX1D overexpression in CD4+ T cells impaired regulatory T cell homeostasis and expanded inflammatory CD4+ T cells. In this study, we showed that PBX1 message expression is downregulated by activation in CD4+ T cells as well as in B cells. PBX1D protein was less stable than the normal isoform, PBX1B, and it is degraded through the ubiquitin-proteasome-dependent pathway. The DNA binding domain lacking in PBX1D has two putative ubiquitin binding sites, K292 and K293, that are predicted to be in direct contact with DNA. Mutation of K292-293 reduced PBX1B stability to a level similar to PBX1D and abrogated DNA binding. In addition, contrary to PBX1B, PBX1D is retained in the cytoplasm without the help of the cofactors MEIS or PREP1, indicating a different requirement for nuclear translocation. Overall, these findings suggest that multiple post-transcriptional mechanisms are responsible for PBX1D loss of function and induction of CD4+ T cell inflammatory phenotypes in systemic lupus erythematosus.Pre-B cell leukemia homeobox 1 (PBX1) controls chromatin accessibility to a large number of genes in various cell types. Its dominant negative splice isoform, PBX1D, which lacks the DNA and Hox-binding domains, is expressed more frequently in the CD4+ T cells from lupus-prone mice and patients with systemic lupus erythematosus than healthy control subjects. PBX1D overexpression in CD4+ T cells impaired regulatory T cell homeostasis and expanded inflammatory CD4+ T cells. In this study, we showed that PBX1 message expression is downregulated by activation in CD4+ T cells as well as in B cells. PBX1D protein was less stable than the normal isoform, PBX1B, and it is degraded through the ubiquitin-proteasome-dependent pathway. The DNA binding domain lacking in PBX1D has two putative ubiquitin binding sites, K292 and K293, that are predicted to be in direct contact with DNA. Mutation of K292-293 reduced PBX1B stability to a level similar to PBX1D and abrogated DNA binding. In addition, contrary to PBX1B, PBX1D is retained in the cytoplasm without the help of the cofactors MEIS or PREP1, indicating a different requirement for nuclear translocation. Overall, these findings suggest that multiple post-transcriptional mechanisms are responsible for PBX1D loss of function and induction of CD4+ T cell inflammatory phenotypes in systemic lupus erythematosus. Pre-B cell leukemia homeobox1 (PBX1) controls chromatin accessibility to large number of genes in various cell types. Its dominant negative splice isoform, PBX1D, which lacks the DNA and Hox-binding domains, is expressed more frequently in the CD4 + T cells from lupus-prone mice and SLE patients than healthy controls. PBX1D overexpression in CD4 + T cells impaired Treg cell homeostasis and expanded inflammatory CD4 + T cells. Here, we showed that PBX1 message expression is downregulated by activation in CD4 + T cells as well as in B cells. PBX1D protein was less stable than the normal isoform, PBX1B, and it is degraded through the ubiquitin-proteasome dependent pathway. The DNA binding domain lacking in PBX1D has two putative ubiquitin binding sites, K292 and K293, that are predicted to be in direct contact with DNA. Mutation of K292–293 reduced PBX1B stability to a level similar to PBX1D and abrogated DNA binding. In addition, contrary to PBX1B, PBX1D is retained in the cytoplasm without the help of the cofactors MEIS or PREP1, indicating a different requirement for nuclear translocation. Overall, these findings suggest that multiple post-transcriptional mechanisms are responsible for PBX1D loss of function and induction of CD4 + T cell inflammatory phenotypes in SLE. |
| Author | Ostrov, David A Park, Yuk Pheel Roach, Tracoyia Choi, Seung-Chul Morel, Laurence Soh, Sujung Yang, Young Zeumer-Spataro, Leilani |
| AuthorAffiliation | 1 Department of Microbiology, Immunology, and Molecular Genetics, University of Texas Health San Antonio, TX 78229-3900, USA 2 Department of Pathology, Immunology and Laboratory Medicine, University of Florida, College of Medicine, Gainesville, FL32610, USA 3 Research Institute of Women’s Health, Sookmyung Women’s University, 100 Cheongparo 47-gil, Yongsan-Gu, Seoul 04310, South Korea, USA |
| AuthorAffiliation_xml | – name: 2 Department of Pathology, Immunology and Laboratory Medicine, University of Florida, College of Medicine, Gainesville, FL32610, USA – name: 3 Research Institute of Women’s Health, Sookmyung Women’s University, 100 Cheongparo 47-gil, Yongsan-Gu, Seoul 04310, South Korea, USA – name: 1 Department of Microbiology, Immunology, and Molecular Genetics, University of Texas Health San Antonio, TX 78229-3900, USA |
| Author_xml | – sequence: 1 givenname: Yuk Pheel orcidid: 0000-0001-9749-5983 surname: Park fullname: Park, Yuk Pheel – sequence: 2 givenname: Tracoyia surname: Roach fullname: Roach, Tracoyia – sequence: 3 givenname: Sujung orcidid: 0000-0001-9576-6524 surname: Soh fullname: Soh, Sujung – sequence: 4 givenname: Leilani surname: Zeumer-Spataro fullname: Zeumer-Spataro, Leilani – sequence: 5 givenname: Seung-Chul surname: Choi fullname: Choi, Seung-Chul – sequence: 6 givenname: David A orcidid: 0000-0002-4696-875X surname: Ostrov fullname: Ostrov, David A – sequence: 7 givenname: Young orcidid: 0000-0003-4239-0804 surname: Yang fullname: Yang, Young – sequence: 8 givenname: Laurence surname: Morel fullname: Morel, Laurence |
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| CitedBy_id | crossref_primary_10_3389_fcell_2024_1372873 crossref_primary_10_1016_j_molimm_2023_11_008 crossref_primary_10_1126_sciadv_adi4310 |
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| Snippet | Pre–B cell leukemia homeobox 1 (PBX1) controls chromatin accessibility to a large number of genes in various cell types. Its dominant negative splice isoform,... Pre-B cell leukemia homeobox 1 (PBX1) controls chromatin accessibility to a large number of genes in various cell types. Its dominant negative splice isoform,... Pre-B cell leukemia homeobox1 (PBX1) controls chromatin accessibility to large number of genes in various cell types. Its dominant negative splice isoform,... |
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| SubjectTerms | Alleles Animals DNA Homeodomain Proteins - genetics Homeodomain Proteins - metabolism Lupus Erythematosus, Systemic - genetics Lupus Erythematosus, Systemic - metabolism Mice Pre-B-Cell Leukemia Transcription Factor 1 - genetics Protein Isoforms - genetics Ubiquitins - genetics |
| Title | Molecular Mechanisms of Lupus Susceptibility Allele PBX1D |
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