Int. J. Dev. Biol. 61: 451 - 457 (2017)

https://doi.org/10.1387/ijdb.170053bc

Vol 61, Issue 6-7

Role of Mad2 expression during the early development of the sea urchin

Developmental Expression Pattern | Published: 11 July 2017

Odile Bronchain¹, Wael Jdey², Laetitia Caraty³ and Brigitte Ciapa¹

¹Paris-Saclay Institute of Neuroscience, CNRS, Univ. Paris-Sud, Université Paris-Saclay, ²Institut Curie, UMR CNRS 3347 and ³Institut de Génétique et Microbiologie, UMR 8621, Université Paris XI, Orsay, France

Abstract

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.

Keywords

Mad2, spindle assembly checkpoint, mitosis, sea urchin, antimitotics