Reactivation at low ATP distinguishes among classes of paralyzed flagella mutants.
Reactivation at low ATP distinguishes among classes of paralyzed flagella mutants.
复制标题
低 ATP 条件下的重新激活可区分不同类别的麻痹鞭毛突变体。
DOI:
10.1002/(sici)1097-0169(1997)38:1
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发表时间:
1997
影响因子:
--
通讯作者:
Omoto,CK
中科院分区:
文献类型:
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作者:
Frey,E;Brokaw,CJ;Omoto,CK
Paralyzed flagella(pf) mutants ofChlamydomonashave been distinguished by the inability of the intact cells to move. Demembranated flagella from these mutants are also immotile when reactivated under standard conditions, with millimolar ATP concentrations. Three of thesepfmutants were previously found to be motile when reactivated under 3 alternate reactivation conditions: low ATP concentration (≦50 μM); 0.1 mM ATP combined with >0.5 mM ADP; or 0.1 mM ATP combined with non‐reactivating ATP analogs anthraniloyl ATP or methylanthraniloyl ATP. We have now surveyed allpfmutants in theChlamydomonasCulture Collection and discovered that a great majority of these mutants can move under these alternate nucleotide conditions. Onlypf22andpf23,mutants missing multiple subsets of dynein arms, did not reactivate under those conditions. This suggests that the paralysis observed in mostpfmutants is the result of inhibition by physiological ATP. Except forpf12,which has an abnormally symmetric bending pattern, all otherpfmutants exhibit asymmetric bending patterns similar to wild‐type. Previously, motility that was restored by the presence of suppressor mutations was found to lack the normal asymmetry of wild‐type flagella or the suppressor by itself. The waveform ofpfmutants at alternate reactivation conditions in the absence of suppressor shows thatpfmutants with radial‐spoke or central‐pair defects are capable of asymmetric bending similar to wild‐type. A complete radial‐spoke/central‐pair complex is not essential for the production of asymmetric bending patterns. Furthermore, this suggests that the symmetric waveform observed previously in suppressedpfmutants is due to the interaction between thepfand suppressor mutations. Cell Motil. Cytoskeleton 38:91–99, 1997. © 1997 Wiley‐Liss, Inc.