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In contrast, these mutant mice formed more structures called cardiac blood islands than a normal mouse.
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Interestingly, presomitic mesoderm retains neuromesodermal plasticity, because Tbx6 mutant mice form two supernumerary neural tubes at the expense of paraxial mesoderm (Chapman and Papaioannou, 1998).
Hydin is not required for cilium formation, as our data reveal that trypanosome Hydin mutants still form a flagellum and hy3 mutant mice form cilia on the ependyma and choroid plexus [ 26].
When the researchers turned the mutant tau on, the mice formed tangles in their hippocampal regions.
Similarly, mutant Myo7a, Ush1c and Cdh23 mice form fewer mechanoreceptor lateral links (Lefèvre et al., 2008), consistent with decreased trafficking of these components.
Consistent with this model, agrin, MuSK and lrp4 mutant mice fail to form NMSs, lacking all features of pre- and postsynaptic specializations [22 24].
β -catenin conditional mutant mice do not form hindlimbs, suggesting that β -catenin is required for hindlimb initiation (Kawakami et al., 2011).
ATG16L1 mutant mice expressed deleted forms of the protein lacking the entire coiled-coil domain [ 99].
LRP5 mutant mice are unable to form a normal vascular capillary network in the deeper plexiform layers of the retina.
Bone marrow MSCs from the mutant mice showed decreased colony forming, cell viability and cell proliferation.
Cells from GMAP210 mutant mice were able to form cilia but they were shorter than normal and contained less polycystin-2 than those detected in control cell lines.
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