Abstract：
:BCL6 is a potent transcriptional repressor that plays important roles in germinal center formation, T helper cell differentiation and lymphomagenesis and regulates expression of several chemokine genes in macrophages. In a further investigation of its role in macrophages, we show that BCL6 inactivation in primary bone marrow-derived macrophages leads to decreased polarization, motility and cell spreading accompanied by an increase in peripheral focal complexes, anchored F-actin bundles and cortical F-actin density. These changes were associated with excess RhoA activation. C3 transferase inhibition of RhoA activity reverted the adhesion structure phenotype, which was not affected by Rho kinase inhibitors, suggesting that other downstream effectors of Rho maintain this Bcl6(-/-) phenotype. Excess RhoA activation in BCL6-deficient macrophages is associated with a decrease in the p120RasGAP (RASA1)-mediated translocation of p190RhoGAP (GRLF1) to active RhoA at the plasma membrane and a reduction in cell surface expression of the CSF1R that has been reported to recruit RasGAP to the plasma membrane. Reconstitution of BCL6 expression in Bcl6(-/-) macrophages results in complete reversion of the morphological phenotype and a significant increase in cell surface CSF1R expression whereas overexpression of the CSF1R corrects the polarization and adhesion structure defects. These results demonstrate that BCL6 suppresses RhoA activity, largely through upregulation of surface CSF1R expression, to modulate cytoskeletal and adhesion structures and increase the motility of macrophages.
journal_name
J Cell Scijournal_title
Journal of cell scienceauthors
Pixley FJ,Xiong Y,Yu RY,Sahai EA,Stanley ER,Ye BHdoi
10.1242/jcs.02314keywords:
subject
Has Abstractpub_date
2005-05-01 00:00:00pages
1873-83issue
Pt 9eissn
0021-9533issn
1477-9137pii
118/9/1873journal_volume
118pub_type
杂志文章abstract：:Transcriptional activation of the major histocompatibility complex (MHC) by IFNgamma is a key step in cell-mediated immunity. At an early stage of IFNgamma induction, chromatin carrying the entire MHC locus loops out from the chromosome 6 territory. We show here that JAK/STAT signalling triggers this higher-order chro...
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journal_title：Journal of cell science
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journal_title：Journal of cell science
pub_type： 杂志文章
doi：
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pub_type： 杂志文章
doi：10.1242/jcs.00380
更新日期：2003-05-01 00:00:00
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journal_title：Journal of cell science
pub_type： 杂志文章
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journal_title：Journal of cell science
pub_type： 杂志文章
doi：
更新日期：1995-01-01 00:00:00
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更新日期：2000-10-01 00:00:00
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doi：
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更新日期：1993-08-01 00:00:00
