EMAGE mouse embryo spatial gene expression database: 2014 update

Richardson, Lorna; Venkataraman, Shanmugasundaram; Stevenson, Peter; Yang, Yiya; Moss, Julie; Graham, Liz; Burton, Nick; Hill, Bill; Rao, Jianguo; Baldock, Richard; Armit, Chris

doi:10.1093/nar/gkt1155

Cited by 131 publications

(113 citation statements)

References 15 publications

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“…Similarly, putting the screen cursor over the image will cause the nearest annotations to be displayed. Selecting a term leaves the flag permanently visible and clicking on a term will provide access to other information and data, in particular the eMouseAtlas (Richardson et al, 2014) and GXD/ MGI (Smith et al, 2014) resources (queried using the EMAPA ID of that tissue) and the licenced material available from Elsevier. In addition, it is possible to inspect the image at high resolution and to make size measurements of any given structure.…”

Section: The Ehistology Resourcementioning

confidence: 99%

The atlas of mouse development eHistology resource

et al. 2015

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The Atlas of Mouse Development by Professor Mathew Kaufman is an essential text for understanding mouse developmental anatomy. This definitive and authoritative atlas is still in production and is essential for any biologist working with the mouse embryo, although the last revision dates back to 1994. Here, we announce the eHistology online resource that provides free access to high-resolution colour images digitized from the original histological sections (www.emouseatlas.org/emap/eHistology/index.php) used by Kaufman for the Atlas. The images are provided with the original annotations and plate numbering of the paper atlas and enable viewing the material to cellular resolution.

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Section: The Ehistology Resourcementioning

confidence: 99%

The atlas of mouse development eHistology resource

et al. 2015

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“…Indeed, embryonic lethality coincides with a lack of induction of MyoD and myogenin at d 14.5 of embryogenesis, suggesting that p300 is required for expression of these myogenic regulatory factors and the development of myogenic precursor cells (13,15). Importantly, in our mKO mouse, it would be expected that KO of p300 would occur before this time point because muscle creatine kinase expression (which drives Cre recombinase in our model) is initially observed by d 13 of embryogenesis and is certainly up-regulated by d 15 (49,50). Therefore, if p300 is required for normal skeletal muscle development, particularly by d 14.5 of embryogenesis, we would expect to see this manifest in the mKO mouse.…”

Section: Discussionmentioning

confidence: 95%

p300 is not required for metabolic adaptation to endurance exercise training

et al. 2015

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The acetyltransferase, E1a-binding protein (p300), is proposed to regulate various aspects of skeletal muscle development, metabolism, and mitochondrial function, via its interaction with numerous transcriptional regulators and other proteins. Remarkably, however, the contribution of p300 to skeletal muscle function and metabolism, in vivo, is poorly understood. To address this, we used Cre-LoxP methodology to generate mice with skeletal muscle-specific knockout of E1a-binding protein (mKO). mKO mice were indistinguishable from their wild-type/ floxed littermates, with no differences in lean mass, skeletal muscle structure, fiber type, respirometry flux, or metabolites of fatty acid and amino acid metabolism. Ex vivo muscle function in extensor digitorum longus and soleus muscles, including peak stress and time to fatigue, as well as in vivo running capacity were also comparable. Moreover, expected adaptations to a 20 d voluntary wheel running regime were not compromised in mKO mice. Taken together, these findings demonstrate that p300 is not required for the normal development or functioning of adult skeletal muscle, nor is it required for endurance exercise-mediated mitochondrial adaptations.-LaBarge,

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“…R26‐mTmG mice (Muzumdar et al ., 2007); obtained from the Jackson Laboratory) and Tie2‐Cre mice (Koni et al ., 2001) were described previously. Staging of E9 and E10 embryos were done by somite counting (sc) and Theiler stage (TS) was determined according to EMAP eMouse Atlas Project (http://www.emouseatlas.org) (Richardson et al ., 2014). Data from E9 embryos refer to sc 15‐18, TS14; E10 sc 24‐26, TS15; and E10.5 sc 34‐37, TS17.…”

Section: Methodsmentioning

confidence: 99%

Pdgfrb‐Cre targets lymphatic endothelial cells of both venous and non‐venous origins

Ulvmar

Martínez-Corral

Stanczuk

et al. 2016

Genesis

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The Pdgfrb‐Cre line has been used as a tool to specifically target pericytes and vascular smooth muscle cells. Recent studies showed additional targeting of cardiac and mesenteric lymphatic endothelial cells (LECs) by the Pdgfrb‐Cre transgene. In the heart, this was suggested to provide evidence for a previously unknown nonvenous source of LECs originating from yolk sac (YS) hemogenic endothelium (HemEC). Here we show that Pdgfrb‐Cre does not, however, target YS HemEC or YS‐derived erythro‐myeloid progenitors (EMPs). Instead, a high proportion of ECs in embryonic blood vessels of multiple organs, as well as venous‐derived LECs were targeted. Assessment of temporal Cre activity using the R26‐mTmG double reporter suggested recent occurrence of Pdgfrb‐Cre recombination in both blood and lymphatic ECs. It thus cannot be excluded that Pdgfrb‐Cre mediated targeting of LECs is due to de novo expression of the Pdgfrb‐Cre transgene or their previously established venous endothelial origin. Importantly, Pdgfrb‐Cre targeting of LECs does not provide evidence for YS HemEC origin of the lymphatic vasculature. Our results highlight the need for careful interpretation of lineage tracing using constitutive Cre lines that cannot discriminate active from historical expression. The early vascular targeting by the Pdgfrb‐Cre also warrants consideration for its use in studies of mural cells. genesis 54:350–358, 2016. © 2016 The Authors. Genesis Published by Wiley Periodicals, Inc.

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EMAGE mouse embryo spatial gene expression database: 2014 update

Cited by 131 publications

References 15 publications

The atlas of mouse development eHistology resource

The atlas of mouse development eHistology resource

p300 is not required for metabolic adaptation to endurance exercise training

Pdgfrb‐Cre targets lymphatic endothelial cells of both venous and non‐venous origins

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