Differential expression of α-fetoprotein genes on the inactive X chromosome in extraembryonic and somatic tissues of a transgenic mouse line

Nature ◽  
1986 ◽  
Vol 319 (6050) ◽  
pp. 224-226 ◽  
Author(s):  
R. Krumlauf ◽  
V. M. Chapman ◽  
R. E. Hammer ◽  
R. Brinster ◽  
S. M. Tilghman



Function ◽  
2021 ◽  
Vol 2 (3) ◽  
Author(s):  
Nelly Redolfi ◽  
Elisa Greotti ◽  
Giulia Zanetti ◽  
Tino Hochepied ◽  
Cristina Fasolato ◽  
...  

AbstractMitochondria play a key role in cellular calcium (Ca2+) homeostasis. Dysfunction in the organelle Ca2+ handling appears to be involved in several pathological conditions, ranging from neurodegenerative diseases, cardiac failure and malignant transformation. In the past years, several targeted green fluorescent protein (GFP)-based genetically encoded Ca2+ indicators (GECIs) have been developed to study Ca2+ dynamics inside mitochondria of living cells. Surprisingly, while there is a number of transgenic mice expressing different types of cytosolic GECIs, few examples are available expressing mitochondria-localized GECIs, and none of them exhibits adequate spatial resolution. Here we report the generation and characterization of a transgenic mouse line (hereafter called mt-Cam) for the controlled expression of a mitochondria-targeted, Förster resonance energy transfer (FRET)-based Cameleon, 4mtD3cpv. To achieve this goal, we engineered the mouse ROSA26 genomic locus by inserting the optimized sequence of 4mtD3cpv, preceded by a loxP-STOP-loxP sequence. The probe can be readily expressed in a tissue-specific manner upon Cre recombinase-mediated excision, obtainable with a single cross. Upon ubiquitous Cre expression, the Cameleon is specifically localized in the mitochondrial matrix of cells in all the organs and tissues analyzed, from embryos to aged animals. Ca2+ imaging experiments performed in vitro and ex vivo in brain slices confirmed the functionality of the probe in isolated cells and live tissues. This new transgenic mouse line allows the study of mitochondrial Ca2+ dynamics in different tissues with no invasive intervention (such as viral infection or electroporation), potentially allowing simple calibration of the fluorescent signals in terms of mitochondrial Ca2+ concentration ([Ca2+]).



2004 ◽  
Vol 13 (2) ◽  
pp. 155-164 ◽  
Author(s):  
Holden Higginbotham ◽  
Stephanie Bielas ◽  
Teruyuki Tanaka ◽  
Joseph G. Gleeson


2018 ◽  
Vol 296 ◽  
pp. 84-92 ◽  
Author(s):  
Christina Pätz ◽  
Simone Brachtendorf ◽  
Jens Eilers


PLoS ONE ◽  
2018 ◽  
Vol 13 (11) ◽  
pp. e0207222 ◽  
Author(s):  
Sandra Schneider ◽  
Nathan Hotaling ◽  
Maria Campos ◽  
Sarita Rani Patnaik ◽  
Kapil Bharti ◽  
...  




PLoS ONE ◽  
2015 ◽  
Vol 10 (6) ◽  
pp. e0129934 ◽  
Author(s):  
Stefanie Besser ◽  
Marit Sicker ◽  
Grit Marx ◽  
Ulrike Winkler ◽  
Volker Eulenburg ◽  
...  


genesis ◽  
2006 ◽  
Vol 44 (6) ◽  
pp. 277-286 ◽  
Author(s):  
Céline Souilhol ◽  
Sarah Cormier ◽  
Marie Monet ◽  
Sandrine Vandormael-Pournin ◽  
Anne Joutel ◽  
...  


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


2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Zhuohao He ◽  
Jennifer D. McBride ◽  
Hong Xu ◽  
Lakshmi Changolkar ◽  
Soo-jung Kim ◽  
...  

AbstractThe deposition of pathological tau is a common feature in several neurodegenerative tauopathies. Although equal ratios of tau isoforms with 3 (3R) and 4 (4R) microtubule-binding repeats are expressed in the adult human brain, the pathological tau from different tauopathies have distinct isoform compositions and cell type specificities. The underlying mechanisms of tauopathies are unknown, partially due to the lack of proper models. Here, we generate a new transgenic mouse line expressing equal ratios of 3R and 4R human tau isoforms (6hTau mice). Intracerebral injections of distinct human tauopathy brain-derived tau strains into 6hTau mice recapitulate the deposition of pathological tau with distinct tau isoform compositions and cell type specificities as in human tauopathies. Moreover, through in vivo propagation of these tau strains among different mouse lines, we demonstrate that the transmission of distinct tau strains is independent of strain isoform compositions, but instead intrinsic to unique pathological conformations.



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