scholarly journals Targeting the Zebrafish Optic Tectum Using In Vivo Electroporation

2010 ◽  
Vol 2010 (7) ◽  
pp. pdb.prot5463-pdb.prot5463 ◽  
Author(s):  
K. J. Hoegler ◽  
J. H. Horne
2015 ◽  
Vol 211 (4) ◽  
pp. 807-814 ◽  
Author(s):  
Sharon R. Cooper ◽  
Michelle R. Emond ◽  
Phan Q. Duy ◽  
Brandon G. Liebau ◽  
Marc A. Wolman ◽  
...  

Cell–cell recognition guides the assembly of the vertebrate brain during development. δ-Protocadherins comprise a family of neural adhesion molecules that are differentially expressed and have been implicated in a range of neurodevelopmental disorders. Here we show that the expression of δ-protocadherins partitions the zebrafish optic tectum into radial columns of neurons. Using in vivo two-photon imaging of bacterial artificial chromosome transgenic zebrafish, we show that pcdh19 is expressed in discrete columns of neurons, and that these columnar modules are derived from proliferative pcdh19+ neuroepithelial precursors. Elimination of pcdh19 results in both a disruption of columnar organization and defects in visually guided behaviors. These results reveal a fundamental mechanism for organizing the developing nervous system: subdivision of the early neuroepithelium into precursors with distinct molecular identities guides the autonomous development of parallel neuronal units, organizing neural circuit formation and behavior.


2014 ◽  
Vol 14 (3) ◽  
pp. 211-217 ◽  
Author(s):  
Xue-Feng Ding ◽  
De-Lin Ma ◽  
Qiang Zhang ◽  
Wei Peng ◽  
Ming Fan ◽  
...  

Function ◽  
2021 ◽  
Author(s):  
Leslie M Baehr ◽  
David C Hughes ◽  
Sarah A Lynch ◽  
Delphi Van Haver ◽  
Teresa Mendes Maia ◽  
...  

Abstract MuRF1 (TRIM63) is a muscle-specific E3 ubiquitin ligase and component of the ubiquitin proteasome system. MuRF1 is transcriptionally upregulated under conditions that cause muscle loss, in both rodents and humans, and is a recognized marker of muscle atrophy. In this study, we used in vivo electroporation to determine if MuRF1 overexpression alone can cause muscle atrophy and, in combination with ubiquitin proteomics, identify the endogenous MuRF1 substrates in skeletal muscle. Overexpression of MuRF1 in adult mice increases ubiquitination of myofibrillar and sarcoplasmic proteins, increases expression of genes associated with neuromuscular junction instability, and causes muscle atrophy. A total of 169 ubiquitination sites on 56 proteins were found to be regulated by MuRF1. MuRF1-mediated ubiquitination targeted both thick and thin filament contractile proteins, as well as, glycolytic enzymes, deubiquitinases, p62, and VCP. These data reveal a potential role for MuRF1 in not only the breakdown of the sarcomere, but also the regulation of metabolism and other proteolytic pathways in skeletal muscle.


2008 ◽  
Vol 82 (11) ◽  
pp. 5643-5649 ◽  
Author(s):  
Jinyan Liu ◽  
Rune Kjeken ◽  
Iacob Mathiesen ◽  
Dan H. Barouch

ABSTRACT In vivo electroporation (EP) has been shown to augment the immunogenicity of plasmid DNA vaccines, but its mechanism of action has not been fully characterized. In this study, we show that in vivo EP augmented cellular and humoral immune responses to a human immunodeficiency virus type 1 Env DNA vaccine in mice and allowed a 10-fold reduction in vaccine dose. This enhancement was durable for over 6 months, and re-exposure to antigen resulted in anamnestic effector and central memory CD8+ T-lymphocyte responses. Interestingly, in vivo EP also recruited large mixed cellular inflammatory infiltrates to the site of inoculation. These infiltrates contained 45-fold-increased numbers of macrophages and 77-fold-increased numbers of dendritic cells as well as 2- to 6-fold-increased numbers of B and T lymphocytes compared to infiltrates following DNA vaccination alone. These data suggest that recruiting inflammatory cells, including antigen-presenting cells (APCs), to the site of antigen production substantially improves the immunogenicity of DNA vaccines. Combining in vivo EP with plasmid chemokine adjuvants that similarly recruited APCs to the injection site, however, did not result in synergy.


2014 ◽  
Vol 13 (1) ◽  
pp. 1270-1277 ◽  
Author(s):  
C.Q. Yang ◽  
X.Y. Li ◽  
Q. Li ◽  
S.L. Fu ◽  
H. Li ◽  
...  

2017 ◽  
Vol 251 (2) ◽  
pp. 211-219 ◽  
Author(s):  
S. Morteza Seyed Jafari ◽  
Maziar Shafighi ◽  
Helmut Beltraminelli ◽  
Benedikt Weber ◽  
Ralph. A. Schmid ◽  
...  

Author(s):  
Kazuya Shimao ◽  
Takuya Takayama ◽  
Katsuhisa Enomoto ◽  
Tetsuya Saito ◽  
Shigenori Nagai ◽  
...  

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