Pottosin Igor, Wherrett Tim, Shabala Sergey
Centro de Investigaciones Biomédicas, Universidad de Colima, Mexico.
FEBS Lett. 2009 Mar 4;583(5):921-6. doi: 10.1016/j.febslet.2009.02.009. Epub 2009 Feb 10.
Vacuoles have long been suggested to mediate a rise in the cytosolic free Ca(2+) during environmental signal transduction. This study addresses the issue of the control of vacuolar calcium release by some of the known signaling molecules such as IP(3), cADPR, ABA, ATP, cAMP, cGMP, H(2)O(2) and CaM. Over 30 concentrations and/or combinations of these signaling compounds were studied in a series of electrophysiological experiments involving non-invasive ion flux measurements (the MIFE) and patch-clamp techniques. Our results suggest that calcium, calmodulin and nucleotides cause calcium release via SV channels.
长期以来,人们一直认为液泡在环境信号转导过程中可介导胞质游离Ca(2+)浓度升高。本研究探讨了一些已知信号分子(如IP(3)、cADPR、ABA、ATP、cAMP、cGMP、H(2)O(2)和CaM)对液泡钙释放的控制问题。在一系列涉及非侵入性离子通量测量(MIFE)和膜片钳技术的电生理实验中,研究了这些信号化合物的30多种浓度和/或组合。我们的结果表明,钙、钙调蛋白和核苷酸通过SV通道引起钙释放。