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Ectopic expression of Gcm1 induces congenital spinal cord abnormalities

Brahim Nait-Oumesmar¹, Barbara Stecca¹, Girish Fatterpekar², Thomas Naidich², Joshua Corbin^1,* and Robert A. Lazzarini^1,

¹ Department of Molecular, Cellular and Developmental Biology and
² Department of Radiology, Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, NY 10029, USA
^* Present address: Skirball Institute, New York University, New York, NY, USA

Author for correspondence (e-mail: robert.lazzarini{at}mssm.edu)

Accepted 9 April 2002

Brief ectopic expression of Gcm1 in mouse embryonic tail bud profoundly affects the development of the nervous system. All mice from 5 independently derived transgenic lines exhibited either one or both of two types of congenital spinal cord pathologies: failure of the neural tube to close (spina bifida) and multiple neural tubes (diastematomyelia). Because the transgene is expressed only in a restricted caudal region and only for a brief interval (E8.5 to E13.5), there was no evidence of embryonic lethality. The dysraphisms develop during the period and within the zone of transgene expression. We present evidence that these dysraphisms result from an inhibition of neuropore closure and a stimulation of secondary neurulation. After transgene expression ceases, the spinal dysraphisms are progressively resolved and the neonatal animals, while showing signs of scarring and tissue resorption, have a closed vertebral column. The multiple spinal cords remain but are enclosed in a single spinal column as in the human diastematomyelia. The animals live a normal life time, are fertile and do not exhibit any obvious weakness or motor disabilities.

Key words: glial cells missing, Secondary neurulation, Cell fate specification, Neural tube defects, Tail bud, Mouse

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