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The miniSOG is a newly engineered fluorescent protein of 106 amino acids that produces singlet oxygen in quantum yield under blue-light illumination. In Caenorhabditis elegans neurons, we transgenically expressed mitochondrially expressed miniSOG. Mito-miniSOG induced neuronal death that seems to be independent of caspase CED-3, but the damaged cells' clearance is partially dependent on the phagocytic receptor CED-1, a homolog of human CD91. Neurons can be killed at various developmental stages, as shown by the figures. Our results support an instructive role for the interneuron AVB in monitoring motor neuron function, as well as an inhibitory effect on the forward interneurons. In summary, the simple inducible cell blation technique used here provides temporal and spatial control and may be a valuable tool in investigating specific cells' function in complex cellular environments.
Active crypt base columnar cells and quiescent +4 cells are among the intestinal epithelium's ability to self-renew and produce differentiated cells that occur in two forms of epithelial stem cells: active crypt base columnar cells and quiescent +4 cells. We investigated the effect of inducing the transcription factor Math1 deletion, an essential source of secretory cell differentiation, here. We discovered that the complete absence of Paneth cells attributed to Math1 deficiency did not alter the crypt structure and allowed the maintenance and dissemination of CBCs. Indeed, Math1-deficient crypt cells survived in vivo Paneth cell death and maintained stable -catenin signaling, but not grow ex vivo without exogenous Wnt, implying that, in vivo, mucosal cells act as a potential niche. Similarly, intestinal tumorigenesis was stimulated by CBC stem cells lacking in adenomatous polyposis coli and Math1 for intestinal proliferation.
To delineate the pancreas, a bioluminescent signal in mice expressing luciferase solely in pancreatic beta cells was used, and it was coregistered with PET and X-ray computed tomography images. Since conditional, specific, and rapid mouse beta-cell ablation, beta-cell loss was detected by bioluminescence imaging, but not by PET imaging, given that the pancreatic signal obtained by three PET radiotracers was not changed. We photographed mice transplanted with luciferase-expressing human islets in vivo to see whether these ligands bound human beta cells in vivo. To determine whether these ligands adhered human beta cells in vivo, we determined that these ligands bound human beta cells in vivo. Bioluminescence images of the human islets were shown by bioluminescence but not with the PET ligands, indicating that these vesicular monoamine transporter 2-directed ligands did not specifically bind beta cells. These results show the value of coregistered multimodal imaging as a tool for testing and proving candidate ligands for imaging islets.
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