XB-IMG-49169
Xenbase Image ID: 49169
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Fig. 1. The KATP channel is necessary for correct left–right patterning. A) Untreated embryo exhibiting normal situs (situs solitus). B–E) Embryos treated with KATP channel blocker HMR-1098 (1.45 mM) ([Dhein et al., 2000], [Edwards et al., 2009], [Jovanovic and Jovanovic, 2005], [Light et al., 2001] and [Suzuki et al., 2003]) from Stage 1 cell to Stage 16 (then washed out into 0.1× MMR and allowed to develop to Stage 46 before being scored for organ situs) exhibit heterotaxia, including B) reversed heart C) reversed heart and gall bladder D) reversed stomach and gall bladder E) Reversed heart, stomach and gall bladder. F–G) Rubidium flux assays of COSm6 cells expressing various KATP subunits. F) xKir6.1 with mouse SUR1 (mSUR1) dramatically increased the rate of efflux compared to untransfected cells by about four-fold, suggesting the formation of function KATP channels. Expression of DNxKir6.1-pore or DNxKir6.1-ER with mouse SUR1 (mSUR1) show that the ER mutant is able to conduct K+ currents with mSUR1, whilst the pore mutant is non-conductive. G,H) DNxKir6.1-pore and DNxKir6.1-ER knock down activity of KATP channels consisting of WTxKir6.1 and mouse SUR1 (F), but not those consisting of mouse Kir6.2 and mouse SUR1 (G). I) Injection of dominant-negatives against xKir6.1 causes significant levels of heterotaxia, but not injection of GFP, or dominant-negative mRNAs against other Kir channels DNKir2.1 (Zobel et al., 2003), DNKir2.2 (Zobel et al., 2003) and DNKir2.3 (Bannister et al., 1999). Image published in: Aw S et al. (2010) Copyright © 2010. Image reproduced with permission of the Publisher, Elsevier B. V. Larger Image Printer Friendly View |