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Luana Soares, Francis Szele and colleagues from Oncology (Eric O’Neill), from Paediatrics (Mathew Wood) and from DPAG (Zoltan Molnar, Mootaz Salman), have identified Galectin-3 as a key regulator of neural development, establishing its contribution to brain growth.

The image shows a coronal section of an embryonic mouse brain with the Galectin-3 protein removed, visualized with immunofluorescence. The cortical neurons (pictured in red and yellow) showcase an emerging groove. The loss of Gal-3 induces abnormal gyrification, or brain tissue folding, in otherwise smooth cortices.
The image shows a coronal section of an embryonic mouse brain with the Galectin-3 protein removed, visualized with immunofluorescence. The cortical neurons (pictured in red and yellow) showcase an emerging groove. The loss of Gal-3 induces abnormal gyrification, or brain tissue folding, in otherwise smooth cortices.

Lead author Luana Soares explained this is the first time that Galectin-3, previously recognized for its role in establishing apical-basal polarity in epithelial cells, has been identified in human neural progenitors, where it plays a vital role in maintaining cellular junctions. She noted that this process is tightly regulated during brain development, and when disrupted, can contribute to neurodevelopmental problems. They blocked Gal-3 genetically and pharmacologically and this caused cortical stem cells to shift their modes of division. Zoltán Molnár noted that the findings demonstrate the power of mouse models for detecting mechanisms for cortical neurogenesis and migration disorders despite considerable differences in the composition and proportions of cortical progenitors and modes of migrations in human brain. The validation of expression patterns in human and the functional tests advise caution that these mechanisms are could be involved in human cortical developmental disorders. 

 

Read the full story on the Department of Physiology, Anatomy and Genetics website.