Published May 2, 2008 | Version v1
Journal article

Microinjection of recombinant O-GlcNAc transferase potentiates Xenopus oocytes M-phase entry

  • 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.2008.02.063

Additional 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.