Imaging approaches to measuring lysosomal calcium

Morgan, Anthony J.; Davis, Lianne C.; Galione, Antony

doi:10.1016/bs.mcb.2014.10.031

Cited by 37 publications

(47 citation statements)

References 99 publications

(130 reference statements)

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“…To confirm that neuronal activity could trigger Ca 2+ release from the lysosomes, we used additional means of pharmacologically impairing lysosomal Ca 2+ signaling (Galione, 2015, Morgan et al., 2015a; Figure 8B). We started by specifically inhibiting lysosomal Ca 2+ storage, which requires a proton gradient to be established by V-ATPases (Morgan et al., 2011).…”

Section: Resultsmentioning

confidence: 99%

Activity-Dependent Exocytosis of Lysosomes Regulates the Structural Plasticity of Dendritic Spines

Padamsey

McGuinness

Bardo

et al. 2017

Neuron

152

151

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SummaryLysosomes have traditionally been viewed as degradative organelles, although a growing body of evidence suggests that they can function as Ca2+ stores. Here we examined the function of these stores in hippocampal pyramidal neurons. We found that back-propagating action potentials (bpAPs) could elicit Ca2+ release from lysosomes in the dendrites. This Ca2+ release triggered the fusion of lysosomes with the plasma membrane, resulting in the release of Cathepsin B. Cathepsin B increased the activity of matrix metalloproteinase 9 (MMP-9), an enzyme involved in extracellular matrix (ECM) remodelling and synaptic plasticity. Inhibition of either lysosomal Ca2+ signaling or Cathepsin B release prevented the maintenance of dendritic spine growth induced by Hebbian activity. This impairment could be rescued by exogenous application of active MMP-9. Our findings suggest that activity-dependent exocytosis of Cathepsin B from lysosomes regulates the long-term structural plasticity of dendritic spines by triggering MMP-9 activation and ECM remodelling.

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Section: Resultsmentioning

confidence: 99%

Activity-Dependent Exocytosis of Lysosomes Regulates the Structural Plasticity of Dendritic Spines

Padamsey

McGuinness

Bardo

et al. 2017

Neuron

152

151

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“…Firstly, although ionomycin is a Ca 2+ -specific ionophore, it is relatively non-selective regarding the membranes into which it can insert. Secondly, Ca 2+ indicator dyes such as Fluo-3 AM can accumulate in secretory vesicles, especially those that are acidic [32].…”

Section: Discussionmentioning

confidence: 99%

Echinochrome A Release by Red Spherule Cells Is an Iron-Withholding Strategy of Sea Urchin Innate Immunity

Coates

McCulloch²,

Betts³

et al. 2017

J Innate Immun

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Cellular immune defences in sea urchins are shared amongst the coelomocytes - a heterogeneous population of cells residing in the coelomic fluid (blood equivalent) and tissues. The most iconic coelomocyte morphotype is the red spherule cell (or amebocyte), so named due to the abundance of cytoplasmic vesicles containing the naphthoquinone pigment echinochrome A. Despite their identification over a century ago, and evidence of antiseptic properties, little progress has been made in characterising the immunocompetence of these cells. Upon exposure of red spherule cells from sea urchins, i.e., Paracentrotus lividus and Psammechinus miliaris, to microbial ligands, intact microbes, and damage signals, we observed cellular degranulation and increased detection of cell-free echinochrome in the coelomic fluid ex vivo. Treatment of the cells with ionomycin, a calcium-specific ionophore, confirmed that an increase in intracellular levels of Ca²⁺ is a trigger of echinochrome release. Incubating Gram-positive/negative bacteria as well as yeast with lysates of red spherule cells led to significant reductions in colony-forming units. Such antimicrobial properties were counteracted by the addition of ferric iron (Fe³⁺), suggesting that echinochrome acts as a primitive iron chelator in echinoid biological defences.

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“…OG-BAP TA (5 µg/ml) fluorescence for each solution was obtained to plot the calibration curve (Christensen et al, 2002;Dickson et al, 2012;Morgan et al, 2015). In cells that were pretreated with ionomycin, nigericin, and valinomycin, in vivo minimal and maximal fluorescence (F min and F max ) were determined by perfusing the cells with 0 or 10 mM Ca 2+ external solutions, respectively (Christensen et al, 2002;Dickson et al, 2012;Morgan et al, 2015). Lysosomal [Ca 2+ ] were at different pH were determined using the following calibration equation: [Ca 2+ ] = K d × (F − F min )/(F max − F).…”

Section: Og-bap Ta Imagingmentioning

confidence: 99%

A voltage-dependent K+ channel in the lysosome is required for refilling lysosomal Ca2+ stores

Wang

Zhang

Gao

et al. 2017

Journal of Cell Biology

108

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Ion-dependent channels and transporters have been identified in lysosomes, including the V-ATPase H+ pump and transient receptor potential mucolipin channels (TRPMLs), the principle Ca2+ release channels in the lysosome, but much less is understood about the roles of Na+ and K+ in lysosomal physiology. Wang et al. describe a voltage-sensitive, Ca2+-activated K+ current in the lysosome (LysoKVCa) and show that LysoKVCa regulates lysosomal membrane potential and refilling of lysosomal Ca2+ stores.

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Imaging approaches to measuring lysosomal calcium

Cited by 37 publications

References 99 publications

Activity-Dependent Exocytosis of Lysosomes Regulates the Structural Plasticity of Dendritic Spines

Activity-Dependent Exocytosis of Lysosomes Regulates the Structural Plasticity of Dendritic Spines

Echinochrome A Release by Red Spherule Cells Is an Iron-Withholding Strategy of Sea Urchin Innate Immunity

A voltage-dependent K+ channel in the lysosome is required for refilling lysosomal Ca2+ stores

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