scholarly journals Distribution and Activity of the Plasma Membrane H+-ATPase in Mimosa pudica L. in Relation to Ionic Fluxes and Leaf Movements

1997 ◽  
Vol 113 (3) ◽  
pp. 747-754 ◽  
Author(s):  
P. Fleurat-Lessard ◽  
S. Bouche-Pillon ◽  
C. Leloup ◽  
J. L. Bonnemain
Keyword(s):  
Plasma Membrane ◽  
Mimosa Pudica ◽  
Ionic Fluxes ◽  
Leaf Movements

Image Processing of Leaf Movements in Mimosa pudica

2017 ◽  
pp. 77-87 ◽  
Author(s):  
Vegard Brattland ◽  
Ivar Austvoll ◽  
Peter Ruoff ◽  
Tormod Drengstig
Keyword(s):  
Image Processing ◽  
Mimosa Pudica ◽  
Leaf Movements

Ionic Channels in Sea Urchin Sperm Physiology

Physiology ◽  
1988 ◽  
Vol 3 (5) ◽  
pp. 181-185
Author(s):  
A Darszon ◽  
A Guerrero ◽  
A Lievano ◽  
M Gonzalez-Martinez ◽  
E Morales
Keyword(s):  
Plasma Membrane ◽  
Sea Urchin ◽  
Acrosome Reaction ◽  
Ionic Channels ◽  
Good Evidence ◽  
Ionic Fluxes ◽  
Sea Urchin Sperm

In sea urchin sperm, ionic fluxes modulate the activation of respiration and motility and the acrosome reaction, a prerequisite for egg fertilization. Ionic channels are present in the plasma membrane of these cells, and there is good evidence indicating that they are deeply involved in these processes.

LEAF MOVEMENTS IN MIMOSA PUDICA L.

1952 ◽  
Vol 50 (3) ◽  
pp. 357-382 ◽  
Author(s):  
MARVIN WEINTRAUB
Keyword(s):  
Mimosa Pudica ◽  
Leaf Movements

scholarly journals NINJ1 mediates plasma membrane rupture during lytic cell death

2020 ◽  
Author(s):  
Nobuhiko Kayagaki ◽  
Opher Kornfeld ◽  
Bettina Lee ◽  
Irma Stowe ◽  
Karen O'Rourke ◽  
...  
Keyword(s):  
Cell Death ◽  
Plasma Membrane ◽  
Apoptotic Cell ◽  
High Mobility ◽  
Surface Protein ◽  
Underlying Mechanism ◽  
Cell Swelling ◽  
Membrane Pore ◽  
Membrane Rupture ◽  
Ionic Fluxes

Abstract Plasma membrane rupture (PMR) is the final cataclysmic event in lytic cell death. PMR releases intracellular molecules termed damage-associated molecular patterns (DAMPs) that propagate the inflammatory response. The underlying mechanism for PMR, however, is unknown. Here we show that the ill-characterized nerve injury-induced protein 1 (NINJ1) — a cell surface protein with two transmembrane regions — plays an essential role in the induction of PMR. A forward-genetic screen of randomly mutagenized mice linked NINJ1 to PMR. Ninj1–/– macrophages exhibited impaired PMR in response to diverse inducers of pyroptotic, necrotic and apoptotic cell death, and failed to release numerous intracellular proteins including High Mobility Group Box 1 (HMGB1, a known DAMP) and Lactate Dehydrogenase (LDH, a standard measure of PMR). Ninj1–/– macrophages died, but with a distinctive and persistent ballooned morphology, attributable to defective disintegration of bubble-like herniations. Ninj1–/– mice were more susceptible than wild-type mice to Citrobacter rodentium, suggesting a role for PMR in anti-bacterial host defense. Mechanistically, NINJ1 utilized an evolutionarily conserved extracellular α-helical domain for oligomerization and subsequent PMR. The discovery of NINJ1 as a mediator of PMR overturns the long-held dogma that cell death-related PMR is a passive event. Pyroptosis is a potent inflammatory mode of lytic cell death triggered by diverse infectious and sterile insults1-3. It is driven by the pore-forming fragment of gasdermin D (GSDMD)4-7 and releases two exemplar proteins: interleukin-1β (IL-1β), a pro-inflammatory cytokine, and LDH, a standard marker of PMR and lytic cell death. An early landmark study8 predicted two sequential steps for pyroptosis: (1) initial formation of a small plasma membrane pore causing IL-1β release and non-selective ionic fluxes, and (2) subsequent PMR attributable to oncotic cell swelling. PMR releases LDH (140 kDa) and large DAMPs. While the predicted size of gasdermin pores (~18 nm inner diameter9) is large enough to release IL-1β (17 kDa, ~4.5 nm diameter), the underlying mechanism for subsequent PMR has been considered a passive osmotic lysis event.

The phenomenon of solar tracking is known from the early studies of Yin (1938) and that it is a blue light response, while the actual photoreceptors involved are not identified (Batschauer 1998; Briggs and Christie, 2002). In view of the fact that solar tracking behaviour results from light-driven turgor changes in the volume of the cells just as in the case of stomatal guard cells, the phototropins might be involved here also (Briggs and Christie, 2002). Sakamoto and Briggs (2002) have suggested that solar tracking may involv e phototropins. The precise molecular mechanisms concernin g the heliotropic movements are not currently known , while some knowledge is available on the mechanism of nyctinastic movements. However, Cronlund and Forseth (1995) have studied the mechanism of soybean leaflet movement and concluded that the mechanism of heliotropic movement was similar to that of nyctinastic movements. These authors have studied the role of K+ channels and the plasma membrane H/ATPase (Michelet and Boutry, 1995) in paraheliotropic movements throug h the measurements of leaf movements after treatment of pulvinus with promoters and inhibitors of HATPase and K+ channels. HATPase inhibition reduced the leaf

2004 ◽  
pp. 101-101
Keyword(s):  
Plasma Membrane ◽  
Molecular Mechanisms ◽  
Light Response ◽  
Guard Cells ◽  
K Channels ◽  
Solar Tracking ◽  
Blue Light Response ◽  
Leaf Movements ◽  
Stomatal Guard Cells
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