The Journal of Neuroscience, December 14, 2005, ():
A Genetic Screen for Mutations That Affect Cranial Nerve Development in the Mouse
J. Neurosci. Mar et al.
25: 11787
Supplemental data
Files in this Data Supplement:
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Supplemental Table 1 Summary of neurodevelopmental mutations recovered
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Supplemental Figure 1. Organization of cranial motor nerves and sensory ganglia in the mouse A. A schematic diagram shows the cranial motor nerves and sensory ganglia of the mouse. Cell bodies of the motor nerves are at different medio-lateral positions within the hindbrain, while those of the sensory ganglia are located flanking the hindbrain. III-oculomotor nerve; IV-the trochlear nerve; V- the trigeminal nerve; VI-the abducens nerve; VII-the facial nerve; VIII-the acoustic nerve; IX- the glossopharyngeal nerve; X-the vagus nerve; XI- the spinal accessory nerve; and XII- the hypoglossal nerve. The IV, VI and XII nerves are somatic motor nerves and have ventrally exiting axons. Axons from the branchiomtor (V, VII, IX, X, XI) and visceromotor (III, VII, IX, X) nerve axons exit the neural tube dorsally in distinct exit points located in the even-numbered rhombomeres or in the case of the oculomotor nerve in the midbrain. Sensory ganglia and motor nerves use the same exit points. Mb-midbrain; fp-floorplate;sc-spinal cord; ov-otic vesicle. (Adapted from Lumsden, 1989 (Lumsden and Keynes, 1989).) B. A sagittal view of a 10.5dpc mouse embryo stained with anti-neurofilament antibody shows the distinct appearance of each cranial ganglia. The oculomotor nerve is marked with an asterisk.
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Supplemental Figure 2. Mutagenesis scheme for recovery of recessive neurodevelopmental mutations.
C57BL/6J male mice were mutagenized with N-ethyl-N-nitrosourea (ENU), and upon recovery of fertility mated with normal C57BL/6J females. Third generation pedigrees were generated for 40 of the resulting G1 male progeny, which were first bred with normal C57Bl/6J mice, and subsequently mated with the resulting G2 daughters. 10.5dpc G3 embryos were harvested from five to seven G2 daughters of each G1 male, and neurodevelopment was analyzed by immunohistochemistry with an anti-neurofilament antibody. A G1 male was designated as carrying a mutation if multiple embryos in multiple litters exhibited the same neuronal abnormality.
