Coronin 1 Regulates Cognition and Behavior through Modulation of cAMP/Protein Kinase A Signaling

Jayachandran, Rajesh; Liu, Xiaolong; BoseDasgupta, Somdeb; Müller, Philipp; Zhang, Chun-Lei; Moshous, Despina; Studer, Vera; Schneider, Jacques; Genoud, Christel; Fossoud, Catherine; Gambino, Frédéric; Khelfaoui, Malik; Müller, Christian; Bartholdi, Deborah; Rossez, Helene; Stieß, Michael; Houbaert, Xander; Jaussi, Rolf; Frey, Daniel; Kammerer, Richard A.; Deupí, Xavier; Villartay, Jean‐Pierre de; Lüthi, Andreas; Humeau, Yann; Pieters, Jean

doi:10.1371/journal.pbio.1001820

Cited by 69 publications

(94 citation statements)

References 89 publications

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“…However, based on our data obtained with T cell-specific Coro1A-deficient mice, we exclude that neuronal Coro1A plays any role in neuronal pathology and axonal injury, which was not very likely. Furthermore, in both mice and humans, a lack of functional Coro1A causes severe neurobehavioral defects, including social deficits, increased aggression, and learning disabilities (26,33). We observed that, in contrast to conventional Coro1a-deficient mice, Cd4-cre ϫ coro1a flox/flox did not display enhanced aggression, which is consistent with the specific absence of Coro1A from T cells (data not shown).…”

Section: Discussionsupporting

confidence: 83%

“…This difference might be attributed to the slightly less efficient deletion of Coro1A expression in CD8 ϩ than CD4 ϩ T cells. Besides its primary expression in the hematopoietic lineage, Coro1A was also detected in neuronal tissue (33,34). However, based on our data obtained with T cell-specific Coro1A-deficient mice, we exclude that neuronal Coro1A plays any role in neuronal pathology and axonal injury, which was not very likely.…”

Section: Discussionmentioning

confidence: 77%

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Proof of Principle for a T Lymphocyte Intrinsic Function of Coronin 1A

Siegmund

Klepsch

Hermann-Kleiter

et al. 2016

Journal of Biological Chemistry

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Coronins are evolutionarily conserved proteins that were originally identified as modulators of actin-dependent processes. Studies analyzing complete Coronin 1a knock-out mice have shown that this molecule is an important regulator of naive T cell homeostasis and it has been linked to immune deficiencies as well as autoimmune disorders. Nevertheless, because Coronin 1A is strongly expressed in all leukocyte subsets, it is not conclusive whether or not this phenotype is attributed to a T cell-intrinsic function of Coronin 1A. To address this research question, we have generated a T cell-specific Coronin 1a knockout mouse (Coro1a fl/fl ؋ Cd4[Cre]). Deletion of Coronin 1A specifically in T cells led to a strong reduction in T cell number and a shift toward the effector/memory phenotype in peripheral lymphoid organs when compared with Cd4[Cre] mice expressing wild-type Coronin 1A. In contrast to peripheral lymphoid tissue, thymocyte number and subsets were not affected by the deletion of Coronin 1a. Furthermore, T cell-specific Coronin 1a knock-out mice were largely resistant to the induction of autoimmunity when tested in the myelin oligoglycoprotein-induced EAE mouse model of multiple sclerosis. Thus, the phenotype of T cell-specific Coronin 1a deletion resembles the phenotype observed with conventional (whole body) Coronin 1a knock-out mice. In summary, our findings provide formal proof of the predominant T cell-intrinsic role of Coronin 1A.

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Section: Discussionsupporting

confidence: 83%

Section: Discussionmentioning

confidence: 77%

Proof of Principle for a T Lymphocyte Intrinsic Function of Coronin 1A

Siegmund

Klepsch

Hermann-Kleiter

et al. 2016

Journal of Biological Chemistry

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“…Multiple previous studies showed an essential role of profiling in long-term potentiation, associated cytoskeletal rearrangement, and importance in memory (127)(128)(129). Involvement of coronin in regulation of synaptic plasticity and cognition was also confirmed (130). Despite the robust network, observation of mild expression level changes indicate that during persistence of memory minor re-arrangement of cytoskeletal components of cellular and synaptic structures may still occur.…”

Section: Discussionmentioning

confidence: 66%

Dynamics of Hippocampal Protein Expression During Long-term Spatial Memory Formation

Borovok

Nesher

Levin

et al. 2016

Molecular & Cellular Proteomics

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Spatial memory depends on the hippocampus, which is particularly vulnerable to aging. This vulnerability has implications for the impairment of navigation capacities in older people, who may show a marked drop in performance of spatial tasks with advancing age. Contemporary understanding of long-term memory formation relies on molecular mechanisms underlying long-term synaptic plasticity. With memory acquisition, activity-dependent changes occurring in synapses initiate multiple signal transduction pathways enhancing protein turnover. This enhancement facilitates de novo synthesis of plasticity related proteins, crucial factors for establishing persistent long-term synaptic plasticity and forming memory engrams. Extensive studies have been performed to elucidate molecular mechanisms of memory traces formation; however, the identity of plasticity related proteins is still evasive. In this study, we investigated protein turnover in mouse hippocampus during long-term spatial memory formation using the reference memory version of radial arm maze (RAM) paradigm. We identified 1592 proteins, which exhibited a complex picture of expression changes during spatial memory formation. Variable linear decomposition reduced significantly data dimensionality and enriched three principal factors responsible for variance of memory-related protein levels at (1) the initial phase of memory acquisition (165 proteins), (2) during the steep learning improvement (148 proteins), and (3) the final phase of the learning curve (123 proteins). Gene ontology and signaling pathways analysis revealed a clear correlation between memory improvement and learning phasecurbed expression profiles of proteins belonging to specific functional categories. We found differential enrichment of (1) Long-term synaptic plasticity is considered a cellular correlate of long-term memory (LTM) 1 . Contemporary understanding of memory formation is based on the initiation and maintenance of long-term synaptic plasticity (1-4), for which de novo protein synthesis is a vital requirement. De novo protein synthesis itself is secondary to activity-dependent changes in synapses that occur during learning processes. These activity changes trigger post-translational modifications of proteins initiating and sustaining multiple signal transduction pathways. In turn, these signaling pathways regulate changes in synaptic strength and connectivity by governing gene expression and protein translation (5-13). Depending on time elapsed since triggering of long-term synaptic plasticity, protein synthesis may be limited to the dendrites directly involved in the plasticity processes (14 -18). Multiple synaptic From the ‡Department

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“…Recent research has implicated the cyclic adenosine monophosphate-protein kinase A-cAMP response elementwww.impactjournals.com/oncotarget/ Oncotarget, Advance Publications 2017 binding protein (cAMP-PKA-CREB) pathway as a key signaling pathway affecting the formation of cognitive function and memory in animals [20][21][22]. This G-coupled receptor signaling pathway involves the activation cAMP which activates PKA and leads to the phosphorylation of CREB.…”

Section: Atrazinementioning

confidence: 99%

WITHDRAWN: Gestational and lactational exposure to atrazine affects behavior and cognitive functions in Sprague-Dawley rats

Li¹,

Yan²,

Li³

et al. 2017

Oncotarget

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The persistence of atrazine in the environment has been linked to neurodegenerative diseases such as Parkinson's disease and Alzheimer's disease. However, to date, there have been few specialized studies demonstrating the effects of atrazine on behavior, learning, and memory, particularly when exposure occurs during early neurodevelopmental stages. Here, using Sprague-Dawley rats, we investigated neurobehavioral and neurochemical effects associated with high and low doses of maternal atrazine exposure at various gestational and postnatal stages. Results indicated that although maternal weight gain and offspring body and brain weights were not significantly affected by atrazine, behavioral tests (including Morris water maze, shuttle box, step down and tensile tests) showed varying degrees of changes between experimental and control groups. Additionally, using transmission electron microscopy, alterations in the hippocampus and hypothalamus were found within affected offspring. Finally we investigated the effects of maternal atrazine exposure on the cAMP-PKA-CREB signaling pathway, as well as interactions between BAI1 and MDM2 on PSD-95 levels. Results suggested that atrazine exposure during gestation and lactation may affect behavioral and cognitive functions in offspring, and there is likely a gender interaction at different doses. In general, male offspring may be more susceptible to this exposure based on behavioral test observations.

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Coronin 1 Regulates Cognition and Behavior through Modulation of cAMP/Protein Kinase A Signaling

Abstract: The evolutionarily conserved protein coronin 1 is needed for activating the cyclic AMP signaling pathway in the brain and is important for cognition and behavior.

Cited by 69 publications

References 89 publications

Proof of Principle for a T Lymphocyte Intrinsic Function of Coronin 1A

Proof of Principle for a T Lymphocyte Intrinsic Function of Coronin 1A

Dynamics of Hippocampal Protein Expression During Long-term Spatial Memory Formation

WITHDRAWN: Gestational and lactational exposure to atrazine affects behavior and cognitive functions in Sprague-Dawley rats

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