Microinjection of recombinant O-GlcNAc transferase potentiates Xenopus oocytes M-phase entry
Creators
- 1. EA 4020, Laboratoire de Regulation des Signaux de Division, USTL, IFR147, Villeneuve d'Ascq (France)
- 2. UMR-CNRS 8576, UGSF, USTL, IFR 147, 59655 Villeneuve d'Ascq (France)
Description
In order to understand the importance of the cytosolic and nuclear-specific O-linked N-acetylglucosaminylation (O-GlcNAc) on cell cycle regulation, we recently reported that inhibition of O-GlcNAc transferase (OGT) delayed or blocked Xenopus laevis oocyte germinal vesicle breakdown (GVBD). Here, we show that increased levels of the long OGT isoform (ncOGT) accelerate X. laevis oocyte GVBD. A N-terminally truncated isoform (sOGT) with a similar in vitro catalytic activity towards a synthetic CKII-derived peptide had no effect, illustrating the important role played by the N-terminal tetratrico-peptide repeats. ncOGT microinjection in the oocytes increases both the speed and extent of O-GlcNAc addition, leads to a quicker activation of the MPF and MAPK pathways and finally results in a faster GVBD. Microinjection of anti-OGT antibodies leads to a delay of the GVBD kinetics. Our results hence demonstrate that OGT is a key molecule for the timely progression of the cell cycle
Availability note (English)
Available from http://dx.doi.org/10.1016/j.bbrc.2008.02.063Additional details
Identifiers
- DOI
- 10.1016/j.bbrc.2008.02.063;
- PII
- S0006-291X(08)00309-4;
Publishing Information
- Journal Title
- Biochemical and Biophysical Research Communications
- Journal Volume
- 369
- Journal Issue
- 2
- Journal Page Range
- p. 539-546
- ISSN
- 0006-291X
- CODEN
- BBRCA9
INIS
- Country of Publication
- United States
- Country of Input or Organization
- International Atomic Energy Agency (IAEA)
- INIS RN
- 40023562
- Subject category
- S60: APPLIED LIFE SCIENCES;
- Descriptors DEI
- ANTIBODIES; CELL CYCLE; GENE REGULATION; IN VITRO; INHIBITION; MOLECULES; OOCYTES; PEPTIDES
- Descriptors DEC
- GERM CELLS; ORGANIC COMPOUNDS; PROTEINS
Optional Information
- Copyright
- Copyright (c) 2008 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.