scholarly journals Cardiac striatin interacts with caveolin-3 and calmodulin in a calcium sensitive manner and regulates cardiomyocyte spontaneous contraction rate

2017 ◽  
Vol 95 (10) ◽  
pp. 1306-1312 ◽  
Author(s):  
Moni Nader ◽  
Shahd Alotaibi ◽  
Ebtehal Alsolme ◽  
Bariaa Khalil ◽  
Ahmed Abu-Zaid ◽  
...  
Keyword(s):  
Myocardial Function ◽  
Spontaneous Contraction ◽  
Contraction Rate ◽  
Atrial Myocardium ◽  
Developmentally Regulated ◽  
Adult Rats ◽  
Binding Domains ◽  
Pulldown Assay ◽  
Neonatal Stage ◽  
Cultured Cardiomyocytes

Impaired cardiomyocyte contraction rate is detrimental to cardiac function and often lethal. Despite advancements in the field, there is a paucity of information regarding the coordination of molecules implicated in regulating the heart rate. Striatin (STRN) is a dynamic protein with binding domains to calmodulin (CaM) and caveolin (Cav), both of which are regulators of myocardial function. However, its role in cardiomyocyte contraction is not yet determined. Herein, we show that STRN is expressed in cardiomyocytes and is more abundant in atrial myocardium than in ventricles. Cardiac expression of STRN (protein and mRNA) was developmentally regulated with the highest expression being at neonatal stage (day one) and the lowest in adult rats (13 weeks). CaM pulldown assay indicated that the interaction of cardiac STRN with CaM and caveolin-3 (Cav-3) was calcium sensitive. Interestingly, the overexpression of STRN induced an increase (∼2-fold) in the rate of the spontaneous contraction of cultured cardiomyocytes, while the knockdown of STRN reduced their contraction rate (∼40%). The expression level of STRN was inversely proportional to the interaction of Cav-3 with the CaM/STRN complex. Collectively, our data delineate a novel role for STRN in regulating cardiomyocyte spontaneous contraction rate and the dynamics of the STRN/Cav-3/CaM complex.

Developmentally regulated expression of a human "finger"-containing gene encoded by the 5' half of the ret transforming gene

1988 ◽  
Vol 8 (4) ◽  
pp. 1853-1856
Author(s):  
M Takahashi ◽  
Y Inaguma ◽  
H Hiai ◽  
F Hirose
Keyword(s):  
Human Gene ◽  
Mrna Levels ◽  
Nucleic Acid Binding ◽  
Developmentally Regulated ◽  
Unique Transcript ◽  
Binding Domains ◽  
Regulated Expression ◽  
Pachytene Spermatocytes ◽  
Human Finger ◽  
Transforming Gene

We isolated and sequenced a cDNA clone of the human gene encoded by the 5' half of the ret transforming gene. The nucleotide sequence indicates that it encodes a protein with "finger" structures which represent putative metal- and nucleic acid-binding domains. Transcription of this gene was detected at high levels in a variety of human and rodent tumor cell lines, mouse testis, and embryos. In addition, a unique transcript was observed in testis RNA. When the expression of the unique transcript was examined at different stages of spermatogenesis, a striking increase in mRNA levels accompanied progression from meiotic prophase pachytene spermatocytes to postmeiotic round spermatids. This finger-containing gene may thus function in male germ cell development.

Stimulation at 1-5 Hz does not produce long-term depression or depotentiation in the hippocampus of the adult rat in vivo

1995 ◽  
Vol 74 (4) ◽  
pp. 1793-1799 ◽  
Author(s):  
M. L. Errington ◽  
T. V. Bliss ◽  
G. Richter-Levin ◽  
K. Yenk ◽  
V. Doyere ◽  
...  
Keyword(s):  
Young Animal ◽  
Low Frequency ◽  
Long Term Depression ◽  
Developmentally Regulated ◽  
Adult Rats ◽  
Adult Rat ◽  
Area Ca1 ◽  
Awake Rat

1. We examined the efficacy of low-frequency trains (1-5 Hz) in producing long-term depression (LTD) or depotentiation in the hippocampus of the awake adult rat and in anesthetized rats aged from 10 days to 3 mo. 2. In the dentate gyrus we found no evidence that low-frequency trains produce either depotentiation or LTD in the awake, adult animal or in the anesthetized animal at any age tested (10 days-adult). 3. In area CA1 of both awake and anesthetized adult rats, we also found no evidence that low-frequency trains induced either LTD or depotentiation. Only in area CA1 of very young rats (10-11 days) was clear evidence for LTD and depotentiation obtained; at this age experiments were only possible in anesthetized animals. By 16 days, the ability to display both LTD and depotentiation was lost. 4. These experiments suggest that repetitive low-frequency stimulation evokes a developmentally regulated form of activity-dependent depression that in the hippocampus is limited to specific pathways in the young animal. Our results leave open the question of whether alternative patterns of activity can induce LTD and/or depotentiation in the adult awake rat.

scholarly journals Identity of the NMDA receptor coagonist is synapse specific and developmentally regulated in the hippocampus

2014 ◽  
Vol 112 (2) ◽  
pp. E204-E213 ◽  
Author(s):  
Matildé Le Bail ◽  
Magalie Martineau ◽  
Silvia Sacchi ◽  
Natalia Yatsenko ◽  
Inna Radzishevsky ◽  
...  
Keyword(s):  
Postnatal Development ◽  
Long Term Potentiation ◽  
Synaptic Activity ◽  
Subunit Composition ◽  
Perforant Path ◽  
Acid Oxidase ◽  
Amino Acid Oxidase ◽  
Developmentally Regulated ◽  
Adult Rats ◽  
Term Potentiation

NMDA receptors (NMDARs) require the coagonists d-serine or glycine for their activation, but whether the identity of the coagonist could be synapse specific and developmentally regulated remains elusive. We therefore investigated the contribution of d-serine and glycine by recording NMDAR-mediated responses at hippocampal Schaffer collaterals (SC)–CA1 and medial perforant path–dentate gyrus (mPP–DG) synapses in juvenile and adult rats. Selective depletion of endogenous coagonists with enzymatic scavengers as well as pharmacological inhibition of endogenous d-amino acid oxidase activity revealed that d-serine is the preferred coagonist at SC–CA1 mature synapses, whereas, unexpectedly, glycine is mainly involved at mPP–DG synapses. Nevertheless, both coagonist functions are driven by the levels of synaptic activity as inferred by recording long-term potentiation generated at both connections. This regional compartmentalization in the coagonist identity is associated to different GluN1/GluN2A to GluN1/GluN2B subunit composition of synaptic NMDARs. During postnatal development, the replacement of GluN2B- by GluN2A-containing NMDARs at SC–CA1 synapses parallels a change in the identity of the coagonist from glycine to d-serine. In contrast, NMDARs subunit composition at mPP–DG synapses is not altered and glycine remains the main coagonist throughout postnatal development. Altogether, our observations disclose an unprecedented relationship in the identity of the coagonist not only with the GluN2 subunit composition at synaptic NMDARs but also with astrocyte activity in the developing and mature hippocampus that reconciles the complementary functions of d-serine and glycine in modulating NMDARs during the maturation of tripartite glutamatergic synapses.

scholarly journals P3495Striatin regulates the dynamics of the Caveolin-3/Calmodulin complex and modulates cardiomyocyte spontaneous contraction rate

2017 ◽  
Vol 38 (suppl_1) ◽  
Author(s):  
M. Nader ◽  
S. Alotaibi ◽  
E. Alsomale ◽  
D. Bakheet ◽  
N. Dzimiri
Keyword(s):  
Spontaneous Contraction ◽  
Contraction Rate

Spontaneous Apamin-Sensitive Hyperpolarizations in Dopaminergic Neurons of Neonatal Rats

1998 ◽  
Vol 80 (6) ◽  
pp. 3361-3364 ◽  
Author(s):  
Vincent Seutin ◽  
Laurent Massotte ◽  
Jacqueline Scuvée-Moreau ◽  
Albert Dresse
Keyword(s):  
Dopaminergic Neurons ◽  
Aminobutyric Acid ◽  
Tetraacetic Acid ◽  
Intracellular Recordings ◽  
Neonatal Rats ◽  
Developmentally Regulated ◽  
Adult Rats ◽  
Physiological Properties ◽  
D2 Antagonist ◽  
Recording Electrodes

Seutin, Vincent, Laurent Massotte, Jacqueline Scuvée-Moreau, and Albert Dresse. Spontaneous apamin-sensitive hyperpolarizations in dopaminergic neurons of neonatal rats. J. Neurophysiol. 80: 3361–3364, 1998. Intracellular recordings from substantia nigra slices revealed the existence of spontaneous hyperpolarizations (amplitude 2–8 mV, duration 100–400 ms) at −60 mV in most dopaminergic neurons of neonatal (9–15 days) but not adult rats. These events were blocked by apamin (300 nM) and bicuculline methochloride (100–300 μM), which blocks apamin-sensitive currents. They were unaffected by the selective γ-aminobutyric acid-A (GABAA) antagonists SR95531 (100 μM) and picrotoxin (30–50 μM), the GABAB antagonist CGP35348 (300 μM), the D2 antagonist haloperidol (1 μM), and the metabotropic antagonist MCPG (1 mM). The hyperpolarizations were strongly attenuated or abolished when recording electrodes contained 200 mM 1,2-bis(2-aminophenoxy)ethane- N, N, N′, N′-tetraacetic acid. They were resistant to tetrodotoxin in the majority of the cells. They had some voltage dependency and were in some cases transiently potentiated when cells were briefly depolarized by current injection. We conclude that dopaminergic neurons have developmentally regulated physiological properties. These spontaneous hyperpolarizations might affect the firing rate of these cells, which was found to be lower in neonates than in adults.

Distribution and ontogeny of thyrotropin-releasing hormone degrading enzymes in rats

1990 ◽  
Vol 259 (6) ◽  
pp. E787-E791 ◽  
Author(s):  
Y. Fuse ◽  
D. H. Polk ◽  
R. W. Lam ◽  
A. L. Reviczky ◽  
D. A. Fisher
Keyword(s):  
Brain Cortex ◽  
Prolyl Endopeptidase ◽  
Rat Tissues ◽  
Peptidase Activity ◽  
Developmentally Regulated ◽  
Adult Rats ◽  
Adult Rat ◽  
Endopeptidase Activity ◽  
Low Levels ◽  
Lung And Kidney

The distribution and ontogeny of tissue prolyl endopeptidase and pyroglutamyl peptidase I activities were studied in the rat from the 7th day before birth to adulthood. While low levels of prolyl endopeptidase activity were demonstrable in many fetal tissues, activity in brain cortex, hypothalamus, lung, and kidney increased dramatically during the 2 wk after birth, gradually returning to adult levels. In adult rats, levels of tissue prolyl endopeptidase activity were highest in kidney, when compared with the intermediate levels in brain cortex, hypothalamus, and liver. Pyroglutamyl peptidase activity was widely distributed in adult rat tissues with high levels in kidney and liver that exceeded intermediate levels in brain cortex and hypothalamus. Pyroglutamyl peptidase activities in fetal gut, brain, and lung tissue were elevated above adult values. In contrast to the development changes in prolyl endopeptidase activities, pyroglutamyl peptidase activity remained elevated above adult levels only during the first week of life. These results indicate that both prolyl endopeptidase and pyroglutamyl peptidase activities in the rat are developmentally regulated.

scholarly journals BSAP Can Repress Enhancer Activity by Targeting PU.1 Function

2000 ◽  
Vol 20 (6) ◽  
pp. 1911-1922 ◽  
Author(s):  
Shanak Maitra ◽  
Michael Atchison
Keyword(s):  
Transcription Factors ◽  
Cell Differentiation ◽  
Dna Binding ◽  
B Cell ◽  
Transactivation Domain ◽  
B Cell Differentiation ◽  
Developmentally Regulated ◽  
Enhancer Activity ◽  
Dna Binding Domains ◽  
Binding Domains

ABSTRACT PU.1 and BSAP are transcription factors crucial for proper B-cell development. Absence of PU.1 results in loss of B, T, and myeloid cells, while absence of BSAP results in an early block in B-cell differentiation. Both of these proteins bind to the immunoglobulin κ chain 3′ enhancer, which is developmentally regulated during B-cell differentiation. We find here that BSAP can repress 3′ enhancer activity. This repression can occur in plasmacytoma lines or in a non-B-cell line in which the enhancer is activated by addition of the appropriate enhancer binding transcription factors. We show that the transcription factor PU.1 is a target of the BSAP-mediated repression. Although PU.1 and BSAP can physically interact through their respective DNA binding domains, this interaction does not affect DNA binding. When PU.1 function is assayed in isolation on a multimerized PU.1 binding site, BSAP targets a portion of the PU.1 transactivation domain (residues 7 to 30) for repression. The BSAP inhibitory domain (residues 358 to 385) is needed for this repression. Interestingly, the coactivator protein p300 can eliminate this BSAP-mediated repression. We also show that PU.1 can inhibit BSAP transactivation and that this repression requires PU.1 amino acids 7 to 30. Transfection of p300 resulted in only a partial reversal of PU.1-mediated repression of BSAP. When PU.1 function is assayed in the context of the immunoglobulin κ chain 3′ enhancer and associated binding proteins, BSAP represses PU.1 function by a distinct mechanism. This repression does not require the PU.1 transactivation or PEST domains and cannot be reversed by p300 expression. The possible roles of BSAP and PU.1 antagonistic activities in hematopoietic development are discussed.

scholarly journals Drosophila Suppressor of Sable Protein [Su(s)] Promotes Degradation of Aberrant and Transposon-Derived RNAs

2009 ◽  
Vol 29 (20) ◽  
pp. 5590-5603 ◽  
Author(s):  
Yung-Shu Kuan ◽  
Paul Brewer-Jensen ◽  
Wen-Li Bai ◽  
Cedric Hunter ◽  
Carrie B. Wilson ◽  
...  
Keyword(s):  
Rna Binding ◽  
Rna Binding Proteins ◽  
Wild Type ◽  
Developmentally Regulated ◽  
Mrna Accumulation ◽  
Binding Domains ◽  
Nuclear Exosome ◽  
Nascent Transcripts ◽  
Fine Tune ◽  
Nucleotide Region

ABSTRACT RNA-binding proteins act at various stages of gene expression to regulate and fine-tune patterns of mRNA accumulation. One protein in this class is Drosophila Su(s), a nuclear protein that has been previously shown to inhibit the accumulation of mutant transcripts by an unknown mechanism. Here, we have identified several additional RNAs that are downregulated by Su(s). These Su(s) targets include cryptic wild-type transcripts from the developmentally regulated Sgs4 and ng1 genes, noncoding RNAs derived from tandemly repeated αβ/αγ elements within an Hsp70 locus, and aberrant transcripts induced by Hsp70 promoter transgenes inserted at ectopic sites. We used the αβ RNAs to investigate the mechanism of Su(s) function and obtained evidence that these transcripts are degraded by the nuclear exosome and that Su(s) promotes this process. Furthermore, we showed that the RNA binding domains of Su(s) are important for this effect and mapped the sequences involved to a 267-nucleotide region of an αβ element. Taken together, these results suggest that Su(s) binds to certain nascent transcripts and stimulates their degradation by the nuclear exosome.

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