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The development of the human oncogenic EGFR induced Muv model.

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posted on 2012-09-05, 00:20 authored by Young-Ki Bae, Jee Young Sung, Yong-Nyun Kim, Sunshin Kim, Kyeong Man Hong, Heung Tae Kim, Min Sung Choi, Jae Young Kwon, Jaegal Shim

(A) LET-23 and LET-23-based chimeric receptor constructs. All constructs were designed to express each chimeric receptor from the let-23 promoter. (B) The LET-23::hEGFR-TK chimera rescues the vulvaless phenotype of the let-23(sy1) mutant. (C) A comparison of several Muv mutants and the jgIs6 transgenic strain which expresses LET-23::hEGFR-TK[L858R]. C. elegans expressing LET-23::hEGFR-TK[L858R] exhibited a larger pseudovulva compared to let-23(sa62) and let-60(n1700) Muv mutants. (D) Hoechst33342 (H33342) staining of the pseudovulval region in jgIs6 revealed many nuclei. The boxed region of the lower panel is enlarged in the right panel. (E) Expression of a 1° cell marker, CDH-3::GFP in the wild-type worm and jgIs6. CDH-3::GFP is highly expressed both in the vulva and pseudovulva of jgIs6. (F) Expression of 2° vulval cell fate markers in the lin-15 Muv mutant and jgIs6. Reporter genes controlled by promoters of egl-17 and dhs-31 were expressed in the vulva and pseudovulva. Arrowheads indicate normal vulvae and small arrows indicate pseudovulvae. Scale bars, 50 µm.

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