TY  - JOUR
TI  - Role of Mad2 expression during the early development of the sea urchin
AU  - Bronchain, Odile
AU  - Jdey, Wael
AU  - Caraty, Laetitia
AU  - Ciapa, Brigitte
T2  - The International Journal of Developmental Biology
AB  - Mitotic arrest deficient 2 (Mad2) belongs to the spindle assembly checkpoint (SAC), a mechanism that blocks progression of the cell cycle until microtubule attachment to kinetochores is complete. It has been found to be involved in the resistance of cancer cells to “anti-mitotic” drugs such as paclitaxel. Mad2 controls meiotic progression, but its role during sea urchin development had never been investigated. Furthermore, the existence of a SAC in this species had never been proved. The present data show that a Mad2 protein, highly homologous to that of humans, is expressed in this species. Mad2 expression increases during development, becoming confined to the endomesoderm at gastrula stages. The level of Mad2 expression is enhanced in embryos that do not gastrulate after treatment with anti-mitotic drugs, lithium or inhibition of the ERK pathway. Mis-aligned and lagging chromosomes were induced after injection of an anti-Mad2 antibody or a Mad2 morpholino. Our results point to the role of a non-canonical SAC involving Mad2 in the control of mitotic divisions of the sea urchin embryo.
PY  - 2017
DO  - 10.1387/ijdb.170053bc
VL  - 61
IS  - 6-7
SP  - 451
EP  - 457
J2  - Int. J. Dev. Biol.
LA  - en
SN  - 0214-6282
SN  - 1696-3547
UR  - https://ijdb.ehu.eus/article/170053bc
Y2  - 2024/11/24/01:23:24
ER  -