c-jun inhibited the alternative splicing of neuron-specific amyloid precursor protein, but stimulated the non-neuron type one in P19 EC cells.
Three alternative splicing products of amyloid precursor protein (APP), APP770, 751 and 695, were detected in mouse embryonal carcinoma (EC) P19 cells by reverse transcriptase RNA polymerase chain reaction (RT-PCR). Alternative splicing of APP pre-mRNA in P19EC cells was remarkably changed by c-jun transformation. The relative ratio of APP770 encoding exons 7 and 8, non-neuron type, was increased by c-jun transformation, while that of APP 695 not encoding exons 7 and 8, neuron-specific one, was decreased. These results suggested that skipping of exons 7 and 8 was specifically blocked in c-jun transformed cells. APP 695, which increases in P19 EC cells under the culture conditions that induce the neuronal differentiation, did not increase in C2C5 cells under the same conditions, suggesting that c-jun transformed cells were not in the neuronal cell lineage and lost the ability to differentiate into neurons.
Division of Development and Differentiation, National Institute of Neuroscience, Tokyo, Japan.
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Odaka
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Tsukahara
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Momoi
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Momoi
D017398:Alternative Splicing; D016564:Amyloid beta-Protein Precursor / Q000235:genetics*; D000818:Animals; D018236:Carcinoma, Embryonal / Q000378:metabolism; D002471:Cell Transformation, Neoplastic / Q000235:genetics; D005091:Exons; D015870:Gene Expression; D016758:Genes, jun; D051379:Mice; D009474:Neurons / Q000378:metabolism*; D016133:Polymerase Chain Reaction; D012333:RNA, Messenger / Q000378:metabolism; D014407:Tumor Cells, Cultured
D016564:Amyloid beta-Protein Precursor; D012333:RNA, Messenger