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Updated: Feb 26, 2026
The Power of Simplicity: Sea Urchin Embryos as in Vivo Developmental Models for Studying Complex Cell-to-cell Signaling Network Interactions
Published on: February 16, 2017
Role of Mad2 expression during the early development of the sea urchin
Odile Bronchain1, Wael Jdey, Laetitia Caraty
1Paris-Saclay Institute of Neuroscience, CNRS, Univ. Paris-Sud, Université Paris-Saclay, 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.
Insights
Sea urchin embryos utilize a non-canonical spindle assembly checkpoint (SAC) involving Mitotic arrest deficient 2 (Mad2). This Mad2 protein is crucial for controlling mitotic divisions and ensuring proper embryonic development.
Area of Science:
- Developmental Biology
- Cell Cycle Regulation
- Molecular Biology
Background:
- The spindle assembly checkpoint (SAC) ensures accurate chromosome segregation during cell division.
- Mitotic arrest deficient 2 (Mad2) is a key component of the SAC, implicated in cancer drug resistance.
- The role of Mad2 and the existence of a SAC in sea urchin development were previously uninvestigated.
Purpose of the Study:
- To investigate the role of Mad2 in sea urchin embryonic development.
- To determine if a functional SAC exists in sea urchins.
- To characterize Mad2 expression patterns and function during sea urchin embryogenesis.
Main Methods:
- Western blot analysis to detect Mad2 protein expression.
- In ovo manipulation including drug treatments (anti-mitotic drugs, lithium) and pathway inhibition (ERK).
- Microinjection of anti-Mad2 antibodies and Mad2 morpholinos.
- Chromosome alignment and segregation analysis.
Main Results:
- A Mad2 protein homologous to human Mad2 is expressed in sea urchins and its expression increases during development.
- Mad2 expression is upregulated in embryos exhibiting developmental defects (e.g., failed gastrulation) after specific treatments.
- Disruption of Mad2 function led to mitotic errors such as mis-aligned and lagging chromosomes.
Conclusions:
- A non-canonical SAC pathway involving Mad2 plays a critical role in regulating mitotic divisions during sea urchin development.
- Mad2 is essential for maintaining genomic stability and proper embryonic progression in this species.
- These findings provide novel insights into conserved mechanisms of cell cycle control across species.
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01:56Gastrulation