scholarly journals Nkx2.2:Cre knock-in mouse line: A novel tool for pancreas- and CNS-specific gene deletion

genesis ◽  
2013 ◽  
Vol 51 (12) ◽  
pp. 844-851 ◽  
Author(s):  
Dina A. Balderes ◽  
Mark A. Magnuson ◽  
Lori Sussel
genesis ◽  
2010 ◽  
Vol 48 (6) ◽  
pp. 400-406 ◽  
Author(s):  
Hua Yang ◽  
Jean Gan ◽  
Xiaoling Xie ◽  
Min Deng ◽  
Liang Feng ◽  
...  

PLoS ONE ◽  
2013 ◽  
Vol 8 (5) ◽  
pp. e63029 ◽  
Author(s):  
Lucie Klimova ◽  
Jitka Lachova ◽  
Ondrej Machon ◽  
Radislav Sedlacek ◽  
Zbynek Kozmik

2015 ◽  
Vol 113 (2) ◽  
pp. 338-343 ◽  
Author(s):  
Kelli J. Carroll ◽  
Catherine A. Makarewich ◽  
John McAnally ◽  
Douglas M. Anderson ◽  
Lorena Zentilin ◽  
...  

Clustered regularly interspaced short palindromic repeats (CRISPR)-associated (Cas)9 genomic editing has revolutionized the generation of mutant animals by simplifying the creation of null alleles in virtually any organism. However, most current approaches with this method require zygote injection, making it difficult to assess the adult, tissue-specific functions of genes that are widely expressed or which cause embryonic lethality when mutated. Here, we describe the generation of cardiac-specific Cas9 transgenic mice, which express high levels of Cas9 in the heart, but display no overt defects. In proof-of-concept experiments, we used Adeno-Associated Virus 9 (AAV9) to deliver single-guide RNA (sgRNA) that targets the Myh6 locus exclusively in cardiomyocytes. Intraperitoneal injection of postnatal cardiac-Cas9 transgenic mice with AAV9 encoding sgRNA against Myh6 resulted in robust editing of the Myh6 locus. These mice displayed severe cardiomyopathy and loss of cardiac function, with elevation of several markers of heart failure, confirming the effectiveness of this method of adult cardiac gene deletion. Mice with cardiac-specific expression of Cas9 provide a tool that will allow rapid and accurate deletion of genes following a single injection of AAV9-sgRNAs, thereby circumventing embryonic lethality. This method will be useful for disease modeling and provides a means of rapidly editing genes of interest in the heart.


IBRO Reports ◽  
2017 ◽  
Vol 3 ◽  
pp. 9-16 ◽  
Author(s):  
Toshikazu Kakizaki ◽  
Hiroyuki Sakagami ◽  
Kenji Sakimura ◽  
Yuchio Yanagawa

2010 ◽  
Vol 208 (1) ◽  
pp. 41-52 ◽  
Author(s):  
Vijay K. Yadav ◽  
Franck Oury ◽  
Kenji F. Tanaka ◽  
Tiffany Thomas ◽  
Ying Wang ◽  
...  

Recent evidence indicates that leptin regulates appetite and energy expenditure, at least in part by inhibiting serotonin synthesis and release from brainstem neurons. To demonstrate that this pathway works postnatally, we used a conditional, brainstem-specific mouse CreERT2 driver to show that leptin signals in brainstem neurons after birth to decrease appetite by inhibiting serotonin synthesis. Cell-specific gene deletion experiments and intracerebroventricular leptin infusions reveal that serotonin signals in arcuate nuclei of the hypothalamus through the Htr1a receptor to favor food intake and that this serotonin function requires the expression of Creb, which regulates the expression of several genes affecting appetite. Accordingly, a specific antagonist of the Htr1a receptor decreases food intake in leptin-deficient but not in Htr1a−/− mice. Collectively, these results establish that leptin inhibition of serotonin is necessary to inhibit appetite postnatally and provide a proof of principle that selective inhibition of this pathway may be a viable option to treat appetite disorders.


Hypertension ◽  
2017 ◽  
Vol 70 (1) ◽  
pp. 111-118 ◽  
Author(s):  
Kohei Ueda ◽  
Mitsuhiro Nishimoto ◽  
Daigoro Hirohama ◽  
Nobuhiro Ayuzawa ◽  
Wakako Kawarazaki ◽  
...  

Pain ◽  
2005 ◽  
Vol 113 (1) ◽  
pp. 27-36 ◽  
Author(s):  
Caroline L. Stirling ◽  
Greta Forlani ◽  
Mark D. Baker ◽  
John N. Wood ◽  
Elizabeth A. Matthews ◽  
...  

genesis ◽  
2005 ◽  
Vol 41 (2) ◽  
pp. 73-80 ◽  
Author(s):  
Sha Li ◽  
Desheng Chen ◽  
Yves Sauvé ◽  
Jeremy McCandless ◽  
Yu-Jiun Chen ◽  
...  

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