| Id |
Subject |
Object |
Predicate |
Lexical cue |
| T1 |
97-236 |
DRI_Outcome |
denotes |
We demonstrate that ion channels contribute to the regulation of dorsal closure in Drosophila, a model system for cell sheet morphogenesis. |
| T2 |
237-389 |
DRI_Approach |
denotes |
We find that Ca(2+) is sufficient to cause cell contraction in dorsal closure tissues, as UV-mediated release of caged Ca(2+) leads to cell contraction. |
| T3 |
390-541 |
DRI_Outcome |
denotes |
Furthermore, endogenous Ca(2+) fluxes correlate with cell contraction in the amnioserosa during closure, whereas the chelation of Ca(2+) slows closure. |
| T4 |
542-815 |
DRI_Background |
denotes |
Microinjection of high concentrations of the peptide GsMTx4, which is a specific modulator of mechanically gated ion channel function, causes increases in cytoplasmic free Ca(2+) and actomyosin contractility and, in the long term, blocks closure in a dose-dependent manner. |
| T5 |
816-943 |
DRI_Approach |
denotes |
We identify two channel subunits, ripped pocket and dtrpA1 (TrpA1), that play a role in closure and other morphogenetic events. |
| T6 |
944-1125 |
DRI_Background |
denotes |
Blocking channels leads to defects in force generation via failure of actomyosin structures, and impairs the ability of tissues to regulate forces in response to laser microsurgery. |
| T7 |
1126-1284 |
DRI_Outcome |
denotes |
Our results point to a key role for ion channels in closure, and suggest a mechanism for the coordination of force-producing cell behaviors across the embryo. |
