Post-priming actions of ATP on Ca ²⁺ -dependent exocytosis in pancreatic beta cells

Abstract

Medical Sciences. In the article "Activation of protein kinase C correlates with a cardioprotective effect of regular ethanol consumption" by Masami Miyamae, Manuel M. Rodriguez, S. Albert Camacho, Ivan Diamond, Daira Mochly-Rosen, and Vincent M. Figueredo, which appeared in number 14, July 7, 1998, of Proc. Natl. Acad. Sci. USA (95, 8262-8267), the following correction should be noted. On page 8264, an incorrect Fig. 1 was printed. The correct figure and its accompanying legend are reproduced below.Neurobiology. In the article "Caspase-1 is activated in neural cells and tissue with amyotrophic lateral sclerosis-associated mutations in copper-zinc superoxide dismutase" by Piera Pasinelli, David R. Borchelt, Megan K. Houseweart, Don W. Cleveland, and Robert H. Brown, Jr., which appeared in number 26, December 22, 1998, of Proc. Natl. Acad. Sci. USA (95, 15763-15768), the following corrections should be noted. An erroneous version of Fig. 6 was published. The lane indicated as G41D represents lumbo-sacral spinal cord extract from G85R transgenic mice. In Fig. 7a, cell viability is expressed as % of untreated cells and not as % of viability. Physiology FIG. 1. LVDP prior to 45 min of global ischemia and duringreperfusion in four groups of perfused guinea pig hearts (n ϭ 9 for each group): 1, following 8 wk 15% ethanol-derived calories (E); 2, pair-fed controls (‚); 3, following 8 wk of ethanol, before and after 10 mM chelerythrine (F); and 4, pair-fed controls, before and after chelerythrine (s). LVDP recovery is significantly greater in hearts from ethanol-treated animals (P Ͻ 0.05 at each 6-min interval). Chelerythrine abolished ethanol's protective effect on LVDP recovery. Data are presented as mean Ϯ SEM (SEM not included for group 2 but lie well within SEM of groups 3 and 4). 3330Corrections Proc. Natl. Acad. Sci. USA 96 (1999) Communicated by Erwin Neher, Max Planck Institute of Biophysical Chemistry, Goettingen, Germany, November 13, 1998 (received for review August 25, 1998 ABSTRACTThe role of cytosolic ATP in exocytosis was investigated by using amperometric measurement of insulin exocytosis in pancreatic beta cells, which were stimulated with photolysis of caged Ca 2؉ compounds. Insulin exocytosis occurred with two rates. We found that ATP hastened and augmented the exocytosis via selective enhancement of the exocytosis with the faster rate. A nonhydrolysable analog of ATP, adenosine 5-O-(3-thiotriphosphate), which blocks ATPase, was even more effective than ATP, indicating that the phosphorylation event occurred downstream of ATPdependent vesicle transportation and priming. The action of ATP was eliminated by a competitive antagonist of cAMP, and by an inhibitor of adenylate cyclase. These data characterize an ATP sensing mechanism for the Ca 2؉ -dependent exocytosis involving adenylate-cyclase, cAMP-dependent protein kinase, and, possibly, the fusion machinery itself. Thus, the fast exocytotic machinery requires both phosphorylation and Ca 2؉ for the final triggering and likely constitutes a di...

Mechanisms of action of glucagon-like peptide 1 in the pancreas

“…By contrast Takahashi and colleagues have presented experimental evidence for the importance of PKA in fast glucose-induced exocytosis (Kasai et al, 2002;Takahashi et al, 1999). The model they have developed is a rapid and reversible post-priming step in which ATP acts independently of its effects on [Ca 2+ ] or the K ATP channels but requires PKA.…”

Involvement of Actin Polymerization in Vesicle Recruitment at the Calyx of Held Synapse

“…Because ATP-␥S can be used as a substrate for protein kinases (Takahashi et al, 1999), it is unlikely that protein kinases are responsible for its action on the recruitment of the slow vesicles (Kraszewski et al, 1996;Becherer et al, 2001). Furthermore, staurosporine (2 M), a general protein kinase inhibitor, had little effect on the recruitment (n ϭ 6).…”

Multiple kinetic components and the Ca2+ requirements of exocytosis

“…We have also shown that exocytosis of the same type of vesicle, serotonin-loaded LVs, occurs in two phases (mode 1 and mode 2) in pancreatic b-cells (Takahashi et al 1997(Takahashi et al , 1999. The slow component (mode 2) of LV exocytosis was often selectively recorded in a certain population of cells (Takahashi et al 1997), suggesting that the two modes re£ect exocytosis of LVs at distinct fusionready states (¢gure 1b).…”

“…The assumption of one ¢nal fusion step is consistent with the homogeneous appearance of the vesicle population and the apparently shared fates of the individual vesicles in certain cell types. Several regulated steps that contribute to such a sequential mechanism have been identi¢ed: (i) the readily releasable pool of vesicles for Ca 2+ -dependent exocytosis is augmented by previous increases in [Ca 2+ ] i (von Rueden & Neher 1993) and by protein kinase C (Gillis et al 1996) in adrenal chroma¤n cells; (ii) phosphorylation by cAMP-dependent protein kinase is necessary for the ¢nal triggering of Ca 2+ -dependent exocytosis in pancreatic b-cells (Takahashi et al 1999); the observation that the ATPase-resistant analogue, ATPg-S, could substitute for ATP in this action indicates that such phosphorylation regulates exocytosis at a step downstream of MgATP-dependent vesicle transportation and priming.…”

“…However, the recent application of caged-Ca 2+ compounds, which makes it possible to generate instantaneous increases in [Ca 2+ ] i in a spatially homogeneous manner, has revealed many aspects of the ¢ne organization of Ca 2+ -dependent exocytosis (Kaplan & EllisDavies 1988;Neher & Zucker 1993;Thomas et al 1993;Ellis-Davies & Kaplan 1994;Parsons et al 1995;Oberhauser et al 1996;Ellis-Davies 1998). We will provide brief reviews of two aspects of this organization: multiple pools of vesicles and the Ca 2+ dependence of their exocytosis Ninomiya et al 1996Ninomiya et al , 1997Ito et al 1997;Takahashi et al 1997Takahashi et al , 1999Kasai 1999). …”