Fut9 Deficiency Causes Abnormal Neural Development in the Mouse Cerebral Cortex and Retina

Area of Science:

• Neuroscience
• Developmental Biology
• Glycobiology

Background:

• Alpha1,3-fucosyltransferase 9 (Fut9) synthesizes the Lewis X (LeX) epitope, a stem cell marker.
• Fut9-deficient mice exhibit anxiety, but brain structural and cellular changes are unknown.

Purpose of the Study:

• To investigate the spatiotemporal expression of Fut9 and LeX in the brain and retina.
• To determine the role of Fut9 in neural development, particularly in cortical and retinal cell differentiation and migration.

Main Methods:

• In situ hybridization and immunohistochemistry to map Fut9 and LeX expression.
• Birthdating analysis (EdU, BrdU) and in utero electroporation to track neuronal development.
• Analysis of Fut9-deficient (Fut9-/-) mice at postnatal day 0 (P0) and adulthood.

Main Results:

• Fut9-expressing cells in the cortex are associated with specific neuronal markers (Ctip2, TLE4).
• Fut9-/- mice show reduced numbers of early-born neurons (E11.5) in the cortex (layer VI/subplate) and retina (ganglion cell layer).
• This deficit in layer VI/subplate neurons persists into adulthood, impacting excitatory neuron populations.

Conclusions:

• Fut9 is essential for the proper differentiation, migration, and maturation of neural precursor cells.
• The study reveals Fut9's critical role in developing specific neuronal populations in the cortex and retina.