Arginine methylation catalyzed by PRMT1 is required for B cell activation and differentiation

Infantino, Simona; Light, Amanda; O’Donnell, Kristy; Bryant, Vanessa L.; Avery, Danielle T.; Elliott, Michael R.; Tangye, Stuart G.; Belz, Gabrielle T.; Mackay, Fabienne; Richard, Stéphane; Tarlinton, David M.

doi:10.1038/s41467-017-01009-1

Cited by 38 publications

(44 citation statements)

References 42 publications

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“…2B). The observation of B cell maturation defects is consistent with other reports using B cell specific PRMT1 KO mice [17][18][19].…”

Section: Loss Of Prmt1 Affects Terminal Hematopoietic Differentiationsupporting

confidence: 92%

“…Our flow-cytometry analysis showed a significant decrease in the frequency and absolute number of mature B cells in PRMT1 f/f /Mx1-CRE mouse BM, and, consistent with other's results [17], found that mice with a B-cell-specific deletion of PRMT1 display a partial block in B cell development at the pre-B cell stage, confirming that PRMT1 is required for lymphocyte development. Infantino et al [19] undertook an immunology analysis on mice with Prmt1 deletion in mature B cells. Their analysis revealed that PRMT1-catalyzed protein substrate methylation is essential for normal B cell proliferation, differentiation and survival.…”

Section: Discussionmentioning

confidence: 99%

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Protein arginine methyltransferase 1 is required for maintenance of normal adult hematopoiesis

Zhu

Dong

et al. 2019

Int. J. Biol. Sci.

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Protein arginine methyltransferase 1 (PRMT1) is the predominant asymmetric (type I) methyltransferase in mammalian cells. Mounting evidence suggested that PRMT1 is essential to embryonic development and tumor pathogenesis, but its role in normal adult hematopoiesis is less studied. We used a Prmt1 conditional knockout (KO) mouse model to identify the role of PRMT1 in normal adult hematopoiesis. The results indicated that deletion of PRMT1 results in anemia and leukopenia, reducing terminal erythroid and lymphocyte differentiation. Additionally, we found a significant decrease of megakaryocyte progenitors (MkPs) compared with similarly treated littermate control mice. The frequency of short-term hematopoietic stem cells (ST-HSCs) and granulocyte-macrophage progenitors (GMPs) populations were significantly lower in PRMT1 f/f /Mx1-CRE bone marrow (BM) compared with littermate control mice. Importantly, in-vitro replating assays and BM transplantation results revealed that PRMT1 KO results in reduced hematopoietic stem and progenitor cells (HSPCs) self-renewal capacity. Thus, we conclude that PRMT1 is required for hematopoietic differentiation and the competitive fitness of HSPCs, and we believed that PRMT1 serves as a key epigenetic regulator of normal hematopoiesis that occurs throughout life.

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“…2B). The observation of B cell maturation defects is consistent with other reports using B cell specific PRMT1 KO mice [17][18][19].…”

Section: Loss Of Prmt1 Affects Terminal Hematopoietic Differentiationsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Protein arginine methyltransferase 1 is required for maintenance of normal adult hematopoiesis

Zhu

Dong

et al. 2019

Int. J. Biol. Sci.

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“…Typhi infection. These results are in agreement with previous data showing that naïve B- and T-cells are less sensitive to perturbations of arginine methylation than memory cells 33 , 34 . Arginine methylation also controls the strength of cell signaling via γ chain (γc)-family cytokines, including interleukin-2 (IL-2), IL-4, IL-7, IL-9, IL-15, and IL-21 35 , that are essential for T-cell development and function 36 .…”

Section: Discussionsupporting

confidence: 93%

Salmonella enterica serovar Typhi exposure elicits ex vivo cell-type-specific epigenetic changes in human gut cells

Sztein

Bafford

Salerno-Gonçalves

2020

Sci Rep

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Salmonella enterica serovar Typhi ( S . Typhi) causes substantial morbidity and mortality worldwide, particularly among young children. Humans develop an array of mucosal immune responses following S . Typhi infection. Whereas the cellular mechanisms involved in S . Typhi infection have been intensively studied, very little is known about the early chromatin modifications occurring in the human gut microenvironment that influence downstream immune responses. To address this gap in knowledge, cells isolated from human terminal ileum exposed ex vivo to the wild-type S . Typhi strain were stained with a 33-metal-labeled antibody panel for mass cytometry analyses of the early chromatin modifications modulated by S . Typhi. We measured the cellular levels of 6 classes of histone modifications, and 1 histone variant in 11 major cell subsets ( i.e ., B, CD3 + T, CD4 + T, CD8 + T, NK, TCR-γδ, Mucosal associated invariant (MAIT), and NKT cells as well as monocytes, macrophages, and epithelial cells). We found that arginine methylation might regulate the early-differentiation of effector-memory CD4+ T-cells following exposure to S . Typhi. We also found S . Typhi-induced post-translational modifications in histone methylation and acetylation associated with epithelial cells, NKT, MAIT, TCR-γδ, Monocytes, and CD8 + T-cells that are related to both gene activation and silencing.

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“…There is a wide variety of post‐translational modifications that can affect gene expression. While most of histone modifications are located on histone tails, epigenetic modifiers can also modify the histone core itself (eg, H3K79me2) or proteins (such as protein arginine methyltransferases). Histone modifications include: acetylation, methylation, ubiquitination, phosphorylation, SUMOylation and ADP‐ribosylation.…”

Section: Modulation Of Dna Methylation and Histone Modifications Are mentioning

confidence: 99%

Epigenetic regulation of B cell fate and function during an immune response

Zhang

Good-Jacobson

2019

Immunological Reviews

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Summary The humoral immune response requires coordination of molecular programs to mediate differentiation into unique B cell subsets that help clear the infection and form immune memory. Epigenetic modifications are crucial for ensuring that the appropriate genes are transcribed or repressed during B cell differentiation. Recent studies have illuminated the changes in DNA methylation and histone post‐translational modifications that accompany the formation of germinal center and antibody‐secreting cells during an immune response. In particular, the B cell subset‐specific expression and function of DNA methyltransferases and histone‐modifying complexes that mediate epigenome changes have begun to be unravelled. This review will discuss the recent advances in this field, as well as highlight critical questions about the relationship between epigenetic regulation and B cell fate and function that are yet to be answered.

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Arginine methylation catalyzed by PRMT1 is required for B cell activation and differentiation

Cited by 38 publications

References 42 publications

Protein arginine methyltransferase 1 is required for maintenance of normal adult hematopoiesis

Protein arginine methyltransferase 1 is required for maintenance of normal adult hematopoiesis

Salmonella enterica serovar Typhi exposure elicits ex vivo cell-type-specific epigenetic changes in human gut cells

Epigenetic regulation of B cell fate and function during an immune response

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