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Adenylate kinase in sea urchin embryonic cilia

โœ Scribed by Kinukawa, Masashi ;Vacquier, Victor D.


Book ID
102097262
Publisher
John Wiley and Sons
Year
2007
Tongue
English
Weight
336 KB
Volume
64
Category
Article
ISSN
0886-1544

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โœฆ Synopsis


Abstract

Sea urchin embryos swim by ciliary movement. Hypertonic shock causes deciliation and loss of motility. Within 2โ€“4 h, cilia regenerate and the embryos swim again. Regeneration of cilia occurs multiple times. The adenylate kinase (AK) activity of isolated cilia was studied. A 130โ€kDa Spโ€AK isozyme, present in sperm flagella, is also present in embryonic cilia. AK activity is responsible for โˆผ93% of nonmitochondrial ATP regeneration from ADP in embryonic cilia. This is unlike sea urchin sperm flagella, where โˆผ31% of the nonmitochondrial ATP regeneration is from the 130โ€kDa Spโ€AK isozyme and โˆผ69% from the flagellar creatine kinase (Spโ€CK). Embryos were deciliated 1โ€“3 times and after a 2โ€h period of regeneration the major ciliary axonemal proteins such as the tubulins appeared constant in amount. However, a moderate decrease in ATPase activity, and a large decrease of total AK activity, were measured. The decrease in AK activity paralleled the decrease in embryo swimming velocity. Embryos were deciliated once and cilia regeneration followed for 4 h. ATPase activity recovered to control levels by 3 h, but AK activity and swimming velocity remained lower than in controls. Detergent solubility data and kinetic experiments indicate that, in addition to the 130โ€kDa Spโ€AK, there is at least one additional AK isozyme in embryonic cilia. Analysis of the S. purpuratus genome indicates five AK isozymes in addition to the 130โ€kDa Spโ€AK isozyme. Decreased swimming velocity of embryos with regenerated cilia suggests that regenerated cilia are not as functionally perfect as naturally grown cilia. Cell Motil. Cytoskeleton 2007. ยฉ 2007 Wileyโ€Liss, Inc.


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