STIM1 is necessary for store‐operated calcium entry in turning growth cones

Mitchell, Camilla B.; Gasperini, Robert; Small, David H.; Foa, Lisa

doi:10.1111/j.1471-4159.2012.07840.x

Cited by 44 publications

(69 citation statements)

References 57 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Similar elevation of intracellular calcium levels in response to Sema3A treatment was recently reported by Mitchell et al (2012) [51]. We also showed that increase of [Ca 2+ ] i in response to Sema3A is a concentration dependent process, and thus can be important in understanding how axonal growth cones behave in Sema3A concentration gradient.…”

Section: Discussionsupporting

confidence: 90%

“…Our results showed that modification of SERCA activity had no effect on Sema3A induced collapse rate, excluding the refilling of the reticular Ca 2+ store as significant for Sema3A induced growth cone collapse in E15 DRG neurons. Thapsigargin was however recently shown to activate ORAI channels in DRG neurons [51]. In our case such an activation of ORAI with thapsigargin had no effect on Sema3A induced elevation of [Ca 2+ ] i .…”

Section: Discussioncontrasting

confidence: 47%

See 1 more Smart Citation

R-Type Calcium Channels Are Crucial for Semaphorin 3A–Induced DRG Axon Growth Cone Collapse

Treinys

Kaselis

Jover³

et al. 2014

PLoS ONE

View full text Add to dashboard Cite

Semaphorin 3A (Sema3A) is a secreted protein involved in axon path-finding during nervous system development. Calcium signaling plays an important role during axonal growth in response to different guidance cues; however it remains unclear whether this is also the case for Sema3A. In this study we used intracellular calcium imaging to figure out whether Sema3A-induced growth cone collapse is a Ca2+ dependent process. Intracellular Ca2+ imaging results using Fura-2 AM showed Ca2+ increase in E15 mice dorsal root ganglia neurons upon Sema3A treatment. Consequently we analyzed Sema3A effect on growth cones after blocking or modifying intracellular and extracellular Ca2+ channels that are expressed in E15 mouse embryos. Our results demonstrate that Sema3A increased growth cone collapse rate is blocked by the non-selective R- and T- type Ca2+ channel blocker NiCl2 and by the selective R-type Ca2+ channel blocker SNX482. These Ca2+ channel blockers consistently decreased the Sema3A-induced intracellular Ca2+ concentration elevation. Overall, our results demonstrate that Sema3A-induced growth cone collapses are intimately related with increase in intracellular calcium concentration mediated by R-type calcium channels.

show abstract

Section: Discussionsupporting

confidence: 90%

Section: Discussioncontrasting

confidence: 47%

R-Type Calcium Channels Are Crucial for Semaphorin 3A–Induced DRG Axon Growth Cone Collapse

Treinys

Kaselis

Jover³

et al. 2014

PLoS ONE

View full text Add to dashboard Cite

show abstract

“…Many different mechanisms for intracellular Ca 2+ elevation have been discovered, including release from ER stores (CICR and IICR) and entry from extracellular sources (CRAC, SOCE, and voltage-sensitive Ca 2+ channels) [22,33,34,38]. A complex pathway which interprets these intracellular Review Trends in Neurosciences August 2014, Vol.…”

Section: Discussionmentioning

confidence: 99%

“…When ER stores are depleted, the ER-resident stromal interaction molecule 1 (STIM1) localizes to the ER and plasma membrane junctions [31][32][33]. From here, STIM1 facilitates SOCE [34] through store-operated calcium (SOC) channels which utilize transient receptor potential cation (TRPC) channels and ORAI1, and calcium release-activated calcium (CRAC) channels which depend primarily on ORAI1 [33,[35][36][37]. Importantly, STIM1 localization in response to gradients of guidance cues is biased towards the up-gradient side of the growth cone, facilitating propagation of asymmetric Ca 2+ elevations [33].…”

Section: Glossarymentioning

confidence: 99%

Calcium signaling in axon guidance

Sutherland

Pujic

Goodhill

2014

Trends in Neurosciences

View full text Add to dashboard Cite

“…Many genes that were changed in NPCs expressing HDAC2 C262A/C274A were also regulated by NO signaling, including Pdgfc (1.9-fold down-regulated) (32). Interestingly, Stim1 (2.4-fold down-regulated), an endoplasmic reticulum Ca 2+ sensor that influences neuronal development and growth cone turning, also regulates NO synthesis (33,34). Genes involved in transcriptional regulation and chromatin modification, such as Brm, the ATPase subunit of the ATP-dependent chromatin-remodeling complex BAF, were also significantly inhibited (1.8-fold) in NPCs expressing HDAC2 C262A/C274A compared with HDAC2 WT .…”

Section: Discussionmentioning

confidence: 99%

S-nitrosylation of HDAC2 regulates the expression of the chromatin-remodeling factor Brm during radial neuron migration

Nott

Nitarska

Veenvliet

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

Dynamic epigenetic modifications play a key role in mediating the expression of genes required for neuronal development. We previously identified nitric oxide (NO) as a signaling molecule that mediates S-nitrosylation of histone deacetylase 2 (HDAC2) and epigenetic changes in neurons. Here, we show that HDAC2 nitrosylation regulates neuronal radial migration during cortical development. Bead-array analysis performed in the developing cortex revealed that brahma (Brm), a subunit of the ATP-dependent chromatin-remodeling complex BRG/brahma-associated factor, is one of the genes regulated by S-nitrosylation of HDAC2. In the cortex, expression of a mutant form of HDAC2 that cannot be nitrosylated dramatically inhibits Brm expression. Our study identifies NO and HDAC2 nitrosylation as part of a signaling pathway that regulates cortical development and the expression of Brm in neurons.neural development | transcription | nitric oxide synthase | polar morphology | schizophrenia N euronal development relies on a number of sequential events whereby a pool of undifferentiated embryonic progenitor cells gives rise to a variety of highly specialized postmitotic neurons and glia. In the cortex, neuronal and glial cells derive from multipotent neural progenitor cells (NPCs) generated in the ventricular zone (VZ) of the developing brain. NPCs either undergo self-renewal or exit the cell cycle, differentiate into postmitotic neurons, and migrate to the external layers of the cortex (1). Cortical layers are formed between embryonic day 11 (E11) and E18 in an inside-out manner with deep layers formed first, followed by the more superficial layers, and the formation depends on radial neuron migration. Extracellular cues that regulate this process include brain-derived neurotrophic factor (BDNF) (2). Although BDNF and TrkB signaling are not required for neuronal survival in the embryonic cortex, they have been implicated in the regulation of NPC proliferation (3) and radial and tangential neuronal migration (2).In addition to the coordinated expression of nuclear factors that regulate, first, neurogenesis and neuronal migration and, later, promote gliogenesis, epigenetic modifications of both DNA and histones represent fundamental mechanisms by which neurons adapt their transcriptional response to corticogenic cues (4). Histone acetylases and deacetylases (HDACs) are nuclear enzymes that maintain chromatin acetylation in balance, thereby contributing to both transcriptional activation and repression. All HDACs identified so far are present in the nervous system and are often developmentally regulated. For example, the highly homologous HDAC1 and HDAC2 are detected at different stages of neuronal development, with HDAC1 confined to neural stem cells and glia and HDAC2 predominantly expressed in postmitotic neuroblasts and differentiated neurons (5).Although it is now established that many posttranslational modifications of HDACs impact on their activity, there is little evidence directly linking extrinsic stimuli to changes of nucle...

show abstract

STIM1 is necessary for store‐operated calcium entry in turning growth cones

Cited by 44 publications

References 57 publications

R-Type Calcium Channels Are Crucial for Semaphorin 3A–Induced DRG Axon Growth Cone Collapse

R-Type Calcium Channels Are Crucial for Semaphorin 3A–Induced DRG Axon Growth Cone Collapse

Calcium signaling in axon guidance

S-nitrosylation of HDAC2 regulates the expression of the chromatin-remodeling factor Brm during radial neuron migration

Contact Info

Product

Resources

About