scholarly journals N-cadherin regulates molecular organization of excitatory and inhibitory synaptic circuits in adult hippocampus in vivo

Hippocampus ◽  
2014 ◽  
Vol 24 (8) ◽  
pp. 943-962 ◽  
Author(s):  
Jessica S. Nikitczuk ◽  
Shekhar B. Patil ◽  
Bridget A. Matikainen-Ankney ◽  
Joseph Scarpa ◽  
Matthew L. Shapiro ◽  
...  

2005 ◽  
Vol 25 (3) ◽  
pp. 945-957 ◽  
Author(s):  
M. M. Robinson ◽  
G. Yatherajam ◽  
R. T. Ranallo ◽  
A. Bric ◽  
M. R. Paule ◽  
...  

ABSTRACT TFIIA interacts with TFIID via association with TATA binding protein (TBP) and TBP-associated factor 11 (TAF11). We previously identified a mutation in the small subunit of TFIIA (toa2-I27K) that is defective for interaction with TAF11. To further explore the functional link between TFIIA and TAF11, the toa2-I27K allele was utilized in a genetic screen to isolate compensatory mutants in TAF11. Analysis of these compensatory mutants revealed that the interaction between TAF11 and TFIIA involves two distinct regions of TAF11: the highly conserved histone fold domain and the N-terminal region. Cells expressing a TAF11 allele defective for interaction with TFIIA exhibit conditional growth phenotypes and defects in transcription. Moreover, TAF11 imparts changes to both TFIIA-DNA and TBP-DNA contacts in the context of promoter DNA. These alterations appear to enhance the formation and stabilization of the TFIIA-TBP-DNA complex. Taken together, these studies provide essential information regarding the molecular organization of the TAF11-TFIIA interaction and define a mechanistic role for this association in the regulation of gene expression in vivo.



2001 ◽  
Vol 21 (15) ◽  
pp. 5109-5121 ◽  
Author(s):  
Yann-Gaël Gangloff ◽  
Jean-Christophe Pointud ◽  
Sylvie Thuault ◽  
Lucie Carré ◽  
Christophe Romier ◽  
...  

ABSTRACT The RNA polymerase II transcription factor TFIID comprises the TATA binding protein (TBP) and a set of TBP-associated factors (TAFIIs). TFIID has been extensively characterized for yeast, Drosophila, and humans, demonstrating a high degree of conservation of both the amino acid sequences of the constituent TAFIIs and overall molecular organization. In recent years, it has been assumed that all the metazoan TAFIIs have been identified, yet no metazoan homologues of yeast TAFII47 (yTAFII47) and yTAFII65 are known. Both of these yTAFIIs contain a histone fold domain (HFD) which selectively heterodimerizes with that of yTAFII25. We have cloned a novel mouse protein, TAFII140, containing an HFD and a plant homeodomain (PHD) finger, which we demonstrated by immunoprecipitation to be a mammalian TFIID component. TAFII140 shows extensive sequence similarity toDrosophila BIP2 (dBIP2) (dTAFII155), which we also show to be a component of DrosophilaTFIID. These proteins are metazoan homologues of yTAFII47 as their HFDs selectively heterodimerize with dTAFII24 and human TAFII30, metazoan homologues of yTAFII25. We further show that yTAFII65 shares two domains with theDrosophila Prodos protein, a recently described potential dTAFII. These conserved domains are critical for yTAFII65 function in vivo. Our results therefore identify metazoan homologues of yTAFII47 and yTAFII65.



2020 ◽  
Vol 30 (10) ◽  
pp. 5517-5531 ◽  
Author(s):  
Sergei A Kirov ◽  
Ioulia V Fomitcheva ◽  
Jeremy Sword

Abstract Two major pathogenic events that cause acute brain damage during neurologic emergencies of stroke, head trauma, and cardiac arrest are spreading depolarizing waves and the associated brain edema that course across the cortex injuring brain cells. Virtually nothing is known about how spreading depolarization (SD)-induced cytotoxic edema evolves at the ultrastructural level immediately after insult and during recovery. In vivo 2-photon imaging followed by quantitative serial section electron microscopy was used to assess synaptic circuit integrity in the neocortex of urethane-anesthetized male and female mice during and after SD evoked by transient bilateral common carotid artery occlusion. SD triggered a rapid fragmentation of dendritic mitochondria. A large increase in the density of synapses on swollen dendritic shafts implies that some dendritic spines were overwhelmed by swelling or merely retracted. The overall synaptic density was unchanged. The postsynaptic dendritic membranes remained attached to axonal boutons, providing a structural basis for the recovery of synaptic circuits. Upon immediate reperfusion, cytotoxic edema mainly subsides as affirmed by a recovery of dendritic ultrastructure. Dendritic recuperation from swelling and reversibility of mitochondrial fragmentation suggests that neurointensive care to improve tissue perfusion should be paralleled by treatments targeting mitochondrial recovery and minimizing the occurrence of SDs.



eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Thomas Pfeiffer ◽  
Stefanie Poll ◽  
Stephane Bancelin ◽  
Julie Angibaud ◽  
VVG Krishna Inavalli ◽  
...  

Rewiring neural circuits by the formation and elimination of synapses is thought to be a key cellular mechanism of learning and memory in the mammalian brain. Dendritic spines are the postsynaptic structural component of excitatory synapses, and their experience-dependent plasticity has been extensively studied in mouse superficial cortex using two-photon microscopy in vivo. By contrast, very little is known about spine plasticity in the hippocampus, which is the archetypical memory center of the brain, mostly because it is difficult to visualize dendritic spines in this deeply embedded structure with sufficient spatial resolution. We developed chronic 2P-STED microscopy in mouse hippocampus, using a ‘hippocampal window’ based on resection of cortical tissue and a long working distance objective for optical access. We observed a two-fold higher spine density than previous studies and measured a spine turnover of ~40% within 4 days, which depended on spine size. We thus provide direct evidence for a high level of structural rewiring of synaptic circuits and new insights into the structure-dynamics relationship of hippocampal spines. Having established chronic super-resolution microscopy in the hippocampus in vivo, our study enables longitudinal and correlative analyses of nanoscale neuroanatomical structures with genetic, molecular and behavioral experiments.



Neuron ◽  
2000 ◽  
Vol 28 (2) ◽  
pp. 527-536 ◽  
Author(s):  
Arnold J. Heynen ◽  
Elizabeth M. Quinlan ◽  
David C. Bae ◽  
Mark F. Bear


2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Franco L. Lombino ◽  
Mary Muhia ◽  
Jeffrey Lopez-Rojas ◽  
Monika S. Brill ◽  
Edda Thies ◽  
...  

Abstract Microtubule severing regulates cytoskeletal rearrangement underlying various cellular functions. Katanin, a heterodimer, consisting of catalytic (p60) and regulatory (p80) subunits severs dynamic microtubules to modulate several stages of cell division. The role of p60 katanin in the mammalian brain with respect to embryonic and adult neurogenesis is poorly understood. Here, we generated a Katna1 knockout mouse and found that consistent with a critical role of katanin in mitosis, constitutive homozygous Katna1 depletion is lethal. Katanin p60 haploinsufficiency induced an accumulation of neuronal progenitors in the subventricular zone during corticogenesis, and impaired their proliferation in the adult hippocampus dentate gyrus (DG) subgranular zone. This did not compromise DG plasticity or spatial and contextual learning and memory tasks employed in our study, consistent with the interpretation that adult neurogenesis may be associated with selective forms of hippocampal-dependent cognitive processes. Our data identify a critical role for the microtubule-severing protein katanin p60 in regulating neuronal progenitor proliferation in vivo during embryonic development and adult neurogenesis.



2007 ◽  
Vol 1 (5) ◽  
pp. 515-528 ◽  
Author(s):  
Hoonkyo Suh ◽  
Antonella Consiglio ◽  
Jasodhara Ray ◽  
Toru Sawai ◽  
Kevin A. D'Amour ◽  
...  


2011 ◽  
Vol 70 (2) ◽  
pp. 133-146 ◽  
Author(s):  
Hrvoje Lepeduš ◽  
Lidija Begović ◽  
Selma MlinarIć ◽  
Domagoj Šimić ◽  
Ivna Štolfa ◽  
...  

Physiology and biochemistry of leaf bleaching in prematurely aging maple (Acer saccharinumL.) trees. II. Functional and molecular adjustment of PSIIIn the present study we aimed to investigate physiological and molecular mechanisms of photosynthetic performance decline in prematurely aged bleached leaves of silver maple (Acer saccharinumL.) trees. We usedin vivochlorophyllafluorescence measurement to analyze changes in PSII photochemistry, relative abundance of photosynthetic proteins (D1, LHCII, Cytfand Rubisco LSU), relations between chlorophylls and their precursor protochlorophyllide as well as elemental composition of the leaves. Decreases in Al, Cr, Cu, Fe, K, Zn and an increase in S concentrations were found in bleached leaves in comparison to healthy green ones. The bleached leaves were visually expressing symptoms characteristic of Fe deficiency. Further, they had considerably decreased chlorophyll contents and protochlorophyllide contents, overall photosynthetic activity and relative abundance of major photosynthetic proteins. All the results indicate that modifications in the molecular organization of photosynthetic electron-transport chain components in bleached leaves led to functional adaptation of the PSII achieved by modifications of some reaction centres (RCs), turning them from active to dissipative. This provided efficient adaptation of bleached leaves to high-light induced oxidative damage during summer.



2021 ◽  
Author(s):  
Nannan Guo ◽  
Kelsey McDermott ◽  
Yu-Tzu Shih ◽  
Haley Zanga ◽  
Debolina Ghosh ◽  
...  

Experience governs neurogenesis from radial-glial neural stem cells (RGLs) in the adult hippocampus to support memory. Transcription factors in RGLs integrate physiological signals to dictate self-renewal division mode. Whereas asymmetric RGL divisions drive neurogenesis during favorable conditions, symmetric divisions prevent premature neurogenesis while amplifying RGLs to anticipate future neurogenic demands. The identities of transcription factors regulating RGL symmetric self-renewal, unlike those that regulate RGL asymmetric self-renewal, are not known. Here, we show that the transcription factor Kruppel-like factor 9 (Klf9) is elevated in quiescent RGLs and inducible, deletion of Klf9 promotes RGL activation state. Clonal analysis and longitudinal intravital 2-photon imaging directly demonstrate that Klf9 functions as a brake on RGL symmetric self-renewal. In vivo translational profiling of RGLs lacking Klf9 generated a blueprint of RGL symmetric self-renewal for stem cell community. Together, these observations identify Klf9 as a transcriptional regulator of neural stem cell expansion in the adult hippocampus.



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