Dlx5 and Dlx6 can antagonize cell division at the G1/S checkpoint
Abstract Background Dlx5 and Dlx6 stimulate differentiation of diverse progenitors during embryonic development. Their actions as pro-differentiation transcription factors includes the up-regulation of differentiation markers but the extent to which differentiation may also be stimulated by regulati...
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doaj-0e199c14462641a49b137b75b2bc16e52020-11-25T02:28:54ZengBMCBMC Molecular and Cell Biology2661-88502019-04-0120111210.1186/s12860-019-0191-6Dlx5 and Dlx6 can antagonize cell division at the G1/S checkpointRachel K. MacKenzie0Parvathy Ravi Sankar1Andrew J. Bendall2Department of Molecular and Cellular Biology, University of GuelphDepartment of Molecular and Cellular Biology, University of GuelphDepartment of Molecular and Cellular Biology, University of GuelphAbstract Background Dlx5 and Dlx6 stimulate differentiation of diverse progenitors during embryonic development. Their actions as pro-differentiation transcription factors includes the up-regulation of differentiation markers but the extent to which differentiation may also be stimulated by regulation of the cell cycle has not been addressed. Results We document that expression of Dlx5 and Dlx6 antagonizes cell proliferation in a variety of cell types without inducing apoptosis or promoting cell cycle exit. Rather, a variety of evidence indicates that elevated Dlx5 and Dlx6 expression reduces the proportion of cells in S phase and affects the length of the cell cycle. Conclusions Antagonism of S-phase entry by Dlx5 and Dlx6 proteins likely represents a lineage-independent function to effect Dlx-mediated differentiation in multiple progenitor cell types.http://link.springer.com/article/10.1186/s12860-019-0191-6Dlx genesCell cycleCheckpointProliferation |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Rachel K. MacKenzie Parvathy Ravi Sankar Andrew J. Bendall |
spellingShingle |
Rachel K. MacKenzie Parvathy Ravi Sankar Andrew J. Bendall Dlx5 and Dlx6 can antagonize cell division at the G1/S checkpoint BMC Molecular and Cell Biology Dlx genes Cell cycle Checkpoint Proliferation |
author_facet |
Rachel K. MacKenzie Parvathy Ravi Sankar Andrew J. Bendall |
author_sort |
Rachel K. MacKenzie |
title |
Dlx5 and Dlx6 can antagonize cell division at the G1/S checkpoint |
title_short |
Dlx5 and Dlx6 can antagonize cell division at the G1/S checkpoint |
title_full |
Dlx5 and Dlx6 can antagonize cell division at the G1/S checkpoint |
title_fullStr |
Dlx5 and Dlx6 can antagonize cell division at the G1/S checkpoint |
title_full_unstemmed |
Dlx5 and Dlx6 can antagonize cell division at the G1/S checkpoint |
title_sort |
dlx5 and dlx6 can antagonize cell division at the g1/s checkpoint |
publisher |
BMC |
series |
BMC Molecular and Cell Biology |
issn |
2661-8850 |
publishDate |
2019-04-01 |
description |
Abstract Background Dlx5 and Dlx6 stimulate differentiation of diverse progenitors during embryonic development. Their actions as pro-differentiation transcription factors includes the up-regulation of differentiation markers but the extent to which differentiation may also be stimulated by regulation of the cell cycle has not been addressed. Results We document that expression of Dlx5 and Dlx6 antagonizes cell proliferation in a variety of cell types without inducing apoptosis or promoting cell cycle exit. Rather, a variety of evidence indicates that elevated Dlx5 and Dlx6 expression reduces the proportion of cells in S phase and affects the length of the cell cycle. Conclusions Antagonism of S-phase entry by Dlx5 and Dlx6 proteins likely represents a lineage-independent function to effect Dlx-mediated differentiation in multiple progenitor cell types. |
topic |
Dlx genes Cell cycle Checkpoint Proliferation |
url |
http://link.springer.com/article/10.1186/s12860-019-0191-6 |
work_keys_str_mv |
AT rachelkmackenzie dlx5anddlx6canantagonizecelldivisionattheg1scheckpoint AT parvathyravisankar dlx5anddlx6canantagonizecelldivisionattheg1scheckpoint AT andrewjbendall dlx5anddlx6canantagonizecelldivisionattheg1scheckpoint |
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