[Roles of tubulin in endocytosis: their contribution to synaptic vesicle recycling].
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Biomedical subjects
Atsuko Honda
Publications and source records attributed to Atsuko Honda.
Ca2+ influx through distinct routes controls exocytosis and endocytosis at drosophila presynaptic terminals.
Endocytosis of synaptic vesicles follows exocytosis, and both processes require external Ca(2+). However, it is not known whether Ca(2+) influx through one route initiates both processes. At larval Drosophila neuromuscular junctions, we separately measured exocytosis and endocytosis using FM1-43. In a temperature-sensitive Ca(2+) channel mutant, cacophony(TS2), exocytosis induced by high K(+) decreased at nonpermissive temperatures, while endocytosis remained unchanged. In wild-type larvae, a spider toxin, PLTXII, preferentially inhibited exocytosis, whereas the Ca(2+) channel blockers flunarizine and La(3+) selectively depressed endocytosis. None of these blockers affected exocytosis or endocytosis induced by a Ca(2+) ionophore. Evoked synaptic potentials were depressed regardless of stimulus frequency in cacophony(TS2) at nonpermissive temperatures and in wild-type by PLTXII, whereas flunarizine or La(3+) gradually depressed synaptic potentials only during high-frequency stimulation, suggesting depletion of synaptic vesicles due to blockade of endocytosis. In shibire(ts1), a dynamin mutant, flunarizine or La(3+) inhibited assembly of clathrin at the plasma membrane during stimulation without affecting dynamin function.
Animals↗
Impaired vascular endothelium-dependent relaxation in Henoch-Schönlein purpura.
Few reports have focused on vascular endothelial function in children with Henoch-Schönlein purpura (HSP). The purpose of the present study was to assess endothelial function and to follow serial changes from the acute to convalescent phases in children with HSP. Forearm flow-mediated vasodilation was evaluated in 21 patients with HSP, aged 4.0-10.3 years (median 6.2 years), and in 14 control subjects. Vascular dimension, mean velocity, and flow volume were measured by ultrasonography in brachial artery before and after hyperemia, and during incremental infusions of nitroglycerin (0.5, 1.0 microg/kg per min). In the controls, significant increases in dimension, mean velocity, and flow volume were observed in reactive hyperemia ( P<0.01). In contrast, patients in the acute phase of HSP showed a flow velocity profile indicating a highly resistant forearm circulation, and significantly attenuated responses after hyperemia ( P<0.01 vs. control), whereas the responses to nitroglycerin were well preserved. In addition, the impaired hyperemic responses recovered in the convalescent phase, with no significant differences compared with controls. These results clearly suggest that forearm vascular endothelium-dependent relaxation was attenuated in patients with acute HSP.
Acute Disease↗
Serum KL-6 level in newborns with meconium aspiration syndrome.
BACKGROUND: It has been reported that serum KL-6 increases in babies with progressing chronic lung disease (CLD). However, there have been few reports assessing KL-6 in meconium aspiration syndrome (MAS). KL-6 was measured in neonates with respiratory diseases including MAS. METHODS: Thirty-eight neonates with respiratory disease were enrolled in the study. These patients were classified into three groups, 14 patients with respiratory distress syndrome (RDS), 14 with MAS, and 10 with transient tachypnea of the newborn (TTN). The control group consisted of 12 healthy neonates. KL-6 levels were measured 1 day (median) after the birth. In the RDS group, measurement was repeated just prior to 36 weeks' postmenstrual age. RESULTS: The levels of KL-6 were 116 +/- 40 U/mL in the RDS, 281 +/- 138 U/mL in the MAS, and 106 +/- 41 U/mL in the TTN groups. KL-6 levels were significantly higher in the MAS group than in the control group (134 +/- 71 U/mL; P < 0.01). In addition, the levels were significantly higher in those with severe MAS than those with mild MAS (P < 0.05). In patients with RDS, KL-6 increased in patients who developed CLD (P < 0.05), while KL-6 levels did not change in those who did not develop CLD. CONCLUSION: These data confirm the high level of KL-6 in CLD, and suggest that KL-6 is increased in MAS.
Antigens↗
Direct, Ca2+-dependent interaction between tubulin and synaptotagmin I: a possible mechanism for attaching synaptic vesicles to microtubules.
The synaptic vesicle protein synaptotagmin I probably plays important roles in the synaptic vesicle cycle. However, the mechanisms of its action remain unclear. In this study, we have searched for cytoplasmic proteins that interact with synaptotagmin I. We found that the cytoskeletal protein tubulin directly and stoichiometrically bound to recombinant synaptotagmin I. The binding depended on mm Ca(2+), and 1 mol of tubulin dimer bound 2 mol of synaptotagmin I with half-maximal binding at 6.6 microm tubulin. The Ca(2+) dependence mainly resulted from Ca(2+) binding to the Ca(2+) ligands of synaptotagmin I. The C-terminal region of beta-tubulin and both C2 domains of synaptotagmin I were involved in the binding. The YVK motif in the C2 domains of synaptotagmin I was essential for tubulin binding. Tubulin and synaptotagmin I were co-precipitated from the synaptosome extract with monoclonal antibodies to tubulin and SNAP-25 (synaptosome-associated protein of 25 kDa), indicating the presence of tubulin/synaptotagmin I complex and tubulin binding to synaptotagmin I in SNARE (soluble N-ethylmaleimide-sensitive factor attachment protein receptor) complexes. Synaptotagmin I promoted tubulin polymerization and bundled microtubules in the presence of Ca(2+). These results suggest that direct interaction between synaptotagmin I and tubulin provides a mechanism for attaching synaptic vesicles to microtubules in high Ca(2+) concentrations.
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