Gao X, Arlotta P, Macklis JD, Chen J. 2007. Conditional knock-out of beta-catenin in postnatal-born dentate gyrus granule neurons results in dendritic malformation. The Journal of neuroscience : the official journal of the Society for Neuroscience. 27(52):14317-25. Pubmed: 18160639


Neurons are continuously added to the brain throughout life, and these neurons must develop dendritic arbors and functional connections with existing neurons to be integrated into neuronal circuitry. The molecular mechanisms that regulate dendritic development of newborn neurons in the hippocampal dentate gyrus are still unclear. Here, we show that beta-catenin is expressed in newborn granule neurons and in neural progenitor cells in the hippocampal dentate gyrus. Specific knock-out of beta-catenin in newborn neurons, without affecting beta-catenin expression in neural progenitor cells, led to defects in dendritic morphology of these newborn neurons in vivo. Majority of newborn neurons that cannot extend dendrites survive <1 month after they were born. Our results indicate that beta-catenin plays an important role in dendritic development of postnatal-born neurons in vivo, and is therefore essential for the neurogenesis in the postnatal brain.

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Photo of Paola Arlotta

Dr. Arlotta is interested in understanding the molecular laws that govern the birth, differentiation and assembly of the cerebral cortex, the part of the brain that controls how we sense, move and think. She integrates developmental and evolutionary knowledge to investigate therapies for brain repair and for modeling neuropsychiatric disease.

Photo of Jeffrey D. Macklis

Jeffrey Macklis investigates molecular controls and mechanisms over neuron subtype specification, development, diversity, axon guidance-circuit formation, and pathology in the cerebral cortex. His lab seeks to apply developmental controls toward brain and spinal cord regeneration and directed differentiation for in vitro mechanistic modeling using human assembloids.

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