scholarly journals A unique mouse strain expressing Cre recombinase for tissue-specific analysis of gene function in palate and kidney development

genesis ◽  
2007 ◽  
Vol 45 (10) ◽  
pp. 618-624 ◽  
Author(s):  
Yu Lan ◽  
Qingru Wang ◽  
Catherine E. Ovitt ◽  
Rulang Jiang
2020 ◽  
Author(s):  
Minghui Yue ◽  
Yu Lan ◽  
Han Liu ◽  
Zhaoming Wu ◽  
Toru Imamura ◽  
...  

1988 ◽  
Vol 66 (8) ◽  
pp. 1767-1771 ◽  
Author(s):  
Kenneth B. Storey

Changes in the activity of glycogen phosphorylase and the content of fructose-2,6-bisphosphate (F-2, 6-P2) were monitored in tissues of the whelk, Busycotypus canaliculatum, over a 21-h course of environmental anoxia. Tissue-specific responses to anoxia were seen with respect to phosphorylase content: in the radular retractor muscle and foot, the content of phosphorylase a expressed rose rapidly over the initial hours of anoxia (maximal increases were 4.3- and 2.5-fold, respectively) while in the gill, content dropped 2-fold during anoxia. Phosphorylase content was modulated by two mechanisms, changes in the percentage of enzyme in the active a form and changes in the total amount (a + b) of enzyme expressed. Anoxia stimulated a dramatic reduction in F-2,6-P2 content in five tissues. In the ventricle, content fell by 224-fold with a t1/2 of only 35 min. Levels in gill, radular retractor, hepatopancreas, and kidney fell to 2.5–3.5% of control values within the first 8 h of anoxia. F-2,6-P2 content in foot muscle was not altered during anoxia. Changes in glycogen phosphorylase activities and F-2,6-P2 contents help to produce tissue-specific responses of glycolysis to environmental anoxia that acknowledge competing metabolic demands including metabolic rate depression, changes in fuel use, anaerobic energy needs, and carbohydrate use for anabolic purposes.


2013 ◽  
Vol 50 ◽  
pp. 118-130 ◽  
Author(s):  
Joshua P. Vandenbrink ◽  
Ryan E. Hammonds ◽  
Roger N. Hilten ◽  
K.C. Das ◽  
J. Michael Henson ◽  
...  

Endocrinology ◽  
2016 ◽  
Vol 157 (1) ◽  
pp. 245-257 ◽  
Author(s):  
Seiichiro Hirono ◽  
Eun Young Lee ◽  
Shunsuke Kuribayashi ◽  
Takahiro Fukuda ◽  
Naokatsu Saeki ◽  
...  

Abstract Dmbx1 is a brain-specific homeodomain transcription factor expressed primarily during embryogenesis, and its systemic disruption (Dmbx1−/−) in the ICR mouse strain resulted in leanness associated with impaired long-lasting orexigenic effect of agouti-related peptide (AgRP). Because spatial and temporal expression patterns of Dmbx1 change dramatically during embryogenesis, it remains unknown when and where Dmbx1 plays a critical role in energy homeostasis. In the present study, the physiological roles of Dmbx1 were examined by its conditional disruption (Dmbx1loxP/loxP) in the C57BL/6 mouse strain. Although Dmbx1 disruption in fetal brain resulted in neonatal lethality, its disruption by synapsin promoter-driven Cre recombinase, which eliminated Dmbx1 expression postnatally, exempted the mice (Syn-Cre;Dmbx1loxP/loxP mice) from lethality. Syn-Cre;Dmbx1loxP/loxP mice show mild leanness and impaired long-lasting orexigenic action of AgRP, demonstrating the physiological relevance of Dmbx1 in the adult. Visualization of Dmbx1-expressing neurons in adult brain using the mice harboring tamoxifen-inducible Cre recombinase in the Dmbx1 locus (Dmbx1CreERT2/+ mice) revealed Dmbx1 expression in small numbers of neurons in restricted regions, including the lateral parabrachial nucleus (LPB). Notably, c-Fos expression in LPB was increased at 48 hours after AgRP administration in Dmbx1loxP/loxP mice but not in Syn-Cre;Dmbx1loxP/loxP mice. These c-Fos-positive neurons in LPB did not coincide with neurons expressing Dmbx1 or melanocortin 4 receptor but did coincide with those expressing calcitonin gene-related peptide. Accordingly, Dmbx1 in the adult LPB is required for the long-lasting orexigenic effect of AgRP via the neural circuitry involving calcitonin gene-related peptide neurons.


2021 ◽  
Author(s):  
Maira P. Almeida ◽  
Sekhar Kambakam ◽  
Fang Liu ◽  
Zhitao Ming ◽  
Jordan M. Welker ◽  
...  

The ability to regulate gene activity spatially and temporally is essential to investigate cell type specific gene function during development and in postembryonic processes and disease models. The Cre/lox system has been widely used for performing cell and tissue-specific conditional analysis of gene function in zebrafish, but simple and efficient methods for isolation of stable, Cre/lox regulated alleles are lacking. Here we applied our GeneWeld CRISPR/Cas9 short homology-directed targeted integration strategy to generate floxed conditional alleles that provide robust gene knockdown and strong loss of function phenotypes. A universal targeting vector, UFlip, with sites for cloning short 24-48 bp homology arms flanking a floxed mRFP gene trap plus secondary reporter cassette, was integrated into an intron in hdac1, rbbp4, and rb1. Active, gene off orientation hdac1-UFlip-Off and rb1-UFlip-Off integration alleles result in >99% reduction of gene expression in homozygotes and recapitulate known indel loss of function phenotypes. Passive, gene on orientation rbbp4-UFlip-On and rb1-UFlip-On integration alleles do not cause phenotypes in trans-heterozygous combination with an indel mutation. Cre recombinase injection leads to recombination at alternating pairs of loxP and lox2272 sites, inverting and locking the cassette into the active, gene off orientation, and the expected mutant phenotypes. In combination with our endogenous neural progenitor Cre drivers we demonstrate rbbp4-UFlip-On and rb1-UFlip-On gene inactivation phenotypes can be restricted to specific neural cell populations. Replacement of the UFlip mRFP primary reporter gene trap with a 2A-RFP in rbbp4-UFlip-Off, or 2A-KalTA4 in rb1-UFlip-Off, shows strong RFP expression in wild type or UAS:RFP injected embryos, respectively. Together these results validate a simplified approach for efficient isolation of highly mutagenic Cre/lox responsive conditional gene alleles to advance zebrafish Cre recombinase genetics.


2018 ◽  
Vol 7 (7) ◽  
pp. 453-463 ◽  
Author(s):  
Yun Hao ◽  
Kayla Quinnies ◽  
Ronald Realubit ◽  
Charles Karan ◽  
Nicholas P. Tatonetti

2020 ◽  
Vol 128 (5) ◽  
pp. 1227-1239
Author(s):  
C. Brooks Mobley ◽  
Ivan J. Vechetti ◽  
Taylor R. Valentino ◽  
John J. McCarthy

The development of tissue-specific inducible transgenic mice has provided a powerful tool to study gene function and cell biology in almost any tissue of interest at any given time within the animal’s life. The purpose of this review is to describe how to use two different inducible transgenic systems, the Cre-loxP system and the Tet-ON/OFF system, that can be used to study skeletal muscle physiology. Myofiber- and satellite cell-specific Cre-loxP transgenic mice are described as is how these mice can be used to knockout a gene of interest or to deplete satellite cells in adult skeletal muscle, respectively. A myofiber-specific Tet-ON system is described as is how such mice can be used to overexpress a gene of interest or to label myonuclei. How to effectively breed and genotype the transgenic mice are also described in detail. The hope is this review will provide the basic information necessary to facilitate the incorporation of tissue-specific inducible transgenic mice into a skeletal muscle research program.


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