期刊
CELL
卷 102, 期 2, 页码 175-187出版社
CELL PRESS
DOI: 10.1016/S0092-8674(00)00023-4
关键词
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资金
- NEI NIH HHS [R01 EY007042, EY07042] Funding Source: Medline
- NICHD NIH HHS [N01-HD-6-2915] Funding Source: Medline
To test whether kinesin-II is important for transport in the mammalian photoreceptor cilium, and to identify its potential cargoes, we used Cre-loxP mutagenesis to remove the kinesin-II subunit, KIF3A, specifically from photoreceptors. Complete loss of KIF3A caused large accumulations of opsin, arrestin, and membranes within the photoreceptor inner segment, while the localization of cu-transducin was unaffected. Other membrane, organelle, and transport markers, as well as opsin processing appeared normal. Loss of KIF3A ultimately caused apoptotic photoreceptor cell death similar to a known opsin transport mutant. The data suggest that kinesin-II is required to transport opsin and arrestin from the inner to the outer segment and that blocks in this transport pathway lead to photoreceptor cell death as found in retinitis pigmentosa.
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