TRIC-A shapes oscillatory Ca2+ signals by interaction with STIM1/Orai1 complexes

Shrestha, Niroj; Bacsa, Bernadett; Ong, Hwei Ling; Scheruebel, Susanne; Bischof, Helmut; Malli, Roland; Ambudkar, Indu S.

doi:10.1371/journal.pbio.3000700

Cited by 17 publications

(8 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Transcripts of the minor Tmem38b gene were found principally at the beginning of corticogenesis (E11–E13) and then declined ( Figure 3 C). TRIC-A has been shown to co-cluster with STIM1/Orai1 proteins and functions as negative modulator of store-operated Ca channels and oscillatory Ca 2+ signals [ 71 ].…”

Section: Resultsmentioning

confidence: 99%

Transcriptomic Profiling of Ca2+ Transport Systems during the Formation of the Cerebral Cortex in Mice

Bouron

2020

Cells

View full text Add to dashboard Cite

Cytosolic calcium (Ca2+) transients control key neural processes, including neurogenesis, migration, the polarization and growth of neurons, and the establishment and maintenance of synaptic connections. They are thus involved in the development and formation of the neural system. In this study, a publicly available whole transcriptome sequencing (RNA-Seq) dataset was used to examine the expression of genes coding for putative plasma membrane and organellar Ca2+-transporting proteins (channels, pumps, exchangers, and transporters) during the formation of the cerebral cortex in mice. Four ages were considered: embryonic days 11 (E11), 13 (E13), and 17 (E17), and post-natal day 1 (PN1). This transcriptomic profiling was also combined with live-cell Ca2+ imaging recordings to assess the presence of functional Ca2+ transport systems in E13 neurons. The most important Ca2+ routes of the cortical wall at the onset of corticogenesis (E11–E13) were TACAN, GluK5, nAChR β2, Cav3.1, Orai3, transient receptor potential cation channel subfamily M member 7 (TRPM7) non-mitochondrial Na+/Ca2+ exchanger 2 (NCX2), and the connexins CX43/CX45/CX37. Hence, transient receptor potential cation channel mucolipin subfamily member 1 (TRPML1), transmembrane protein 165 (TMEM165), and Ca2+ “leak” channels are prominent intracellular Ca2+ pathways. The Ca2+ pumps sarco/endoplasmic reticulum Ca2+ ATPase 2 (SERCA2) and plasma membrane Ca2+ ATPase 1 (PMCA1) control the resting basal Ca2+ levels. At the end of neurogenesis (E17 and onward), a more numerous and diverse population of Ca2+ uptake systems was observed. In addition to the actors listed above, prominent Ca2+-conducting systems of the cortical wall emerged, including acid-sensing ion channel 1 (ASIC1), Orai2, P2X2, and GluN1. Altogether, this study provides a detailed view of the pattern of expression of the main actors participating in the import, export, and release of Ca2+. This work can serve as a framework for further functional and mechanistic studies on Ca2+ signaling during cerebral cortex formation.

show abstract

Section: Resultsmentioning

confidence: 99%

Transcriptomic Profiling of Ca2+ Transport Systems during the Formation of the Cerebral Cortex in Mice

Bouron

2020

Cells

View full text Add to dashboard Cite

show abstract

“…We observed an increase in oscillation frequency but a decrease in the average amplitude of these oscillations in neurons in the optic tectum in stim2a −/− zebrafish compared with WT fish. It was shown earlier that STIM2 deletion and the subsequent SOCE disruption caused the decrease in oscillations of non-neuronal cells [ 66 , 67 ]. However, our in vivo data showed the increased Ca 2+ oscillation frequency in brain neurons stim2a −/− mutants.…”

Section: Discussionmentioning

confidence: 99%

Knockout of stim2a Increases Calcium Oscillations in Neurons and Induces Hyperactive-Like Phenotype in Zebrafish Larvae

Gupta

Wasilewska

Palchevska

et al. 2020

IJMS

View full text Add to dashboard Cite

Stromal interaction molecule (STIM) proteins play a crucial role in store-operated calcium entry (SOCE) as endoplasmic reticulum Ca2+ sensors. In neurons, STIM2 was shown to have distinct functions from STIM1. However, its role in brain activity and behavior was not fully elucidated. The present study analyzed behavior in zebrafish (Danio rerio) that lacked stim2a. The mutant animals had no morphological abnormalities and were fertile. RNA-sequencing revealed alterations of the expression of transcription factor genes and several members of the calcium toolkit. Neuronal Ca2+ activity was measured in vivo in neurons that expressed the GCaMP5G sensor. Optic tectum neurons in stim2a−/− fish had more frequent Ca2+ signal oscillations compared with neurons in wildtype (WT) fish. We detected an increase in activity during the visual–motor response test, an increase in thigmotaxis in the open field test, and the disruption of phototaxis in the dark/light preference test in stim2a−/− mutants compared with WT. Both groups of animals reacted to glutamate and pentylenetetrazol with an increase in activity during the visual–motor response test, with no major differences between groups. Altogether, our results suggest that the hyperactive-like phenotype of stim2a−/− mutant zebrafish is caused by the dysregulation of Ca2+ homeostasis and signaling.

show abstract

“…Shrestha et al . reported that TRIC-A interacts with the STIM1/Orai1 complex and negatively regulates STIM1/Orai1 function [ 20 ]. They reported that TRIC-A modulates SOCE and oscillatory calcium signals by affecting the STIM1/Orai1 complex.…”

Section: Discussionmentioning

confidence: 99%

Decreased cardiac pacemaking and attenuated β-adrenergic response in TRIC-A knockout mice

et al. 2020

View full text Add to dashboard Cite

Changes in intracellular calcium levels in the sinus node modulate cardiac pacemaking (the calcium clock). Trimeric intracellular cation (TRIC) channels are counterion channels on the surface of the sarcoplasmic reticulum and compensate for calcium release from ryanodine receptors, which play a major role in calcium-induced calcium release (CICR) and the calcium clock. TRIC channels are expected to affect the calcium clock in the sinus node. However, their physiological importance in cardiac rhythm formation remains unclear. We evaluated the importance of TRIC channels on cardiac pacemaking using TRIC-A-null (TRIC-A–/–) as well as TRIC-B+/–mice. Although systolic blood pressure (SBP) was not significantly different between wild-type (WT), TRIC-B+/–, and TRIC-A–/–mice, heart rate (HR) was significantly lower in TRIC-A–/–mice than other lines. Interestingly, HR and SBP showed a positive correlation in WT and TRIC-B+/–mice, while no such correlation was observed in TRIC-A–/–mice, suggesting modification of the blood pressure regulatory system in these mice. Isoproterenol (0.3 mg/kg) increased the HR in WT mice (98.8 ± 15.1 bpm), whereas a decreased response in HR was observed in TRIC-A–/–mice (23.8 ± 5.8 bpm), suggesting decreased sympathetic responses in TRIC-A–/–mice. Electrocardiography revealed unstable R-R intervals in TRIC-A–/–mice. Furthermore, TRIC-A–/–mice sometimes showed sinus pauses, suggesting a significant role of TRIC-A channels in cardiac pacemaking. In isolated atrium contraction or action potential recording, TRIC-A–/–mice showed decreased response to a β-adrenergic sympathetic nerve agonist (isoproterenol, 100 nM), indicating decreased sympathetic responses. In summary, TRIC-A–/–mice showed decreased cardiac pacemaking in the sinus node and attenuated responses to β-adrenergic stimulation, indicating the involvement of TRIC-A channels in cardiac rhythm formation and decreased sympathetic responses.

show abstract

TRIC-A shapes oscillatory Ca2+ signals by interaction with STIM1/Orai1 complexes

Cited by 17 publications

References 42 publications

Transcriptomic Profiling of Ca2+ Transport Systems during the Formation of the Cerebral Cortex in Mice

Transcriptomic Profiling of Ca2+ Transport Systems during the Formation of the Cerebral Cortex in Mice

Knockout of stim2a Increases Calcium Oscillations in Neurons and Induces Hyperactive-Like Phenotype in Zebrafish Larvae

Decreased cardiac pacemaking and attenuated β-adrenergic response in TRIC-A knockout mice

Contact Info

Product

Resources

About