Regulation of reactivated elongation in lysed cell models of teleost retinal cones by cAMP and calcium.
Regulation of reactivated elongation in lysed cell models of teleost retinal cones by cAMP and calcium.
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DOI：
10.1083/jcb.102.3.1047
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发表时间：
1986-03
影响因子：
7.8
通讯作者：
BURNSIDE, B
中科院分区：
文献类型：
--
作者：
GILSON, CA;ACKLAND, N;BURNSIDE, B
硬骨鱼视网膜锥体在黑暗中伸长，在光线下收缩。在绿色太阳鱼Lepomis Bluellus的离休视网膜中，视锥肌样细胞经历微管依赖性的延长，从5微米到45微米。我们之前已经证明，在用Brij-58裂解的锥体的运动模型中，锥体收缩可以重新激活。重新激活的收缩依赖于肌动蛋白和三磷酸腺苷，由钙激活，而被cAMP抑制。我们在这里报告，我们已经在用同样的程序制备的裂解模型中获得了重新激活的锥体伸长。重新激活的延伸率依赖于ATP，由cAMP激活，而被钙抑制。再激活的延长率与cAMP浓度在10微米到0.5 mM之间成正比，但在10微米到1.0 mM mg-ATP之间是恒定的。如果cAMP或mg-ATP浓度小于或等于5微米，则不会发生伸长。无论是cAMP依赖的过程还是cAMP非依赖的过程都需要mg-ATP，这表明mg-ATP既是导致cAMP依赖的磷酸化的调控过程所必需的，也是产生力量的过程所必需的。游离钙浓度大于或等于10(-7)会使延伸率降低78%或更多，完全抑制10(-5)M的延伸率。这种抑制不是由于与钙激活的收缩竞争所致。细胞松弛素D阻断重新激活的收缩，但不能取消钙对重新激活的伸长的抑制。因此，钙直接影响伸长机制。钙抑制作用依赖于钙调蛋白。钙调蛋白抑制剂三氟拉嗪可消除钙对伸长的抑制作用。此外，只有在裂解步骤中存在钙时，钙才会阻止伸长；随后的钙添加没有任何影响。然而，如果随后加入钙和外源钙调蛋白，则伸长再次被抑制。因此，钙抑制似乎需要一种可溶性的钙调蛋白，该蛋白在溶解后不久就会丢失。
Teleost retinal cones elongate in the dark and contract in the light. In isolated retinas of the green sunfish Lepomis cyanellus, cone myoids undergo microtubule-dependent elongation from 5 to 45 micron. We have previously shown that cone contraction can be reactivated in motile models of cones lysed with Brij-58. Reactivated contraction is both actin and ATP dependent, activated by calcium, and inhibited by cAMP. We report here that we have obtained reactivated cone elongation in lysed models prepared by the same procedures. Reactivated elongation is ATP dependent, activated by cAMP, and inhibited by calcium. The rate of reactivated elongation is proportional to the cAMP concentration between 10 microM and 0.5 mM, but is constant between 10 microM and 1.0 mM Mg-ATP. No elongation occurs if cAMP or Mg-ATP concentration is less than or equal to 5 microM. Mg-ATP is required for both cAMP-dependent and cAMP-independent processes, suggesting that Mg-ATP is required both for a regulatory process entailing cAMP-dependent phosphorylation and for a force-producing process. Free calcium concentrations greater than or equal to 10(-7) reduce the elongation rate by 78% or more, completely inhibiting elongation at 10(-5) M. This inhibition is not due to competition from calcium-activated contraction. Cytochalasin D blocks reactivated contraction, but does not abolish calcium inhibition of reactivated elongation. Thus calcium directly affects the elongation mechanism. Calcium inhibition is calmodulin dependent. The calmodulin inhibitor trifluoperazine abolishes calcium inhibition of elongation. Furthermore, calcium blocks elongation only if present during the lysis step; subsequent calcium addition has no effect. However, if calcium plus exogenous calmodulin are subsequently added, elongation is again inhibited. Thus calcium inhibition appears to require a soluble calmodulin which is lost shortly after lysis.
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通过环状腺苷3'，'5-磷酸磷酸盐诱导黑暗视网膜锥体中暗体自适应视网膜运动运动（细胞伸长）。
影响因子：
3.8
作者：
Burnside, B;Evans, M;Fletcher, R T;Chader, G J
通讯作者：
Chader, G J
影响因子：
3.9
作者：
BLUM, JJ;HAYES, A;VANAMAN, TC
通讯作者：
VANAMAN, TC
影响因子：
3.9
作者：
BROKAW, CJ;BENEDICT, B
通讯作者：
BENEDICT, B
影响因子：
3.8
作者：
DEARRY, A;BURNSIDE, B
通讯作者：
BURNSIDE, B
影响因子：
7.8
作者：
GIBBONS, BH;GIBBONS, IR
通讯作者：
GIBBONS, IR