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Moreover, the chitin synthase A in the Bis-SEL strain was clearly up-regulated, and a mutation (H866Y) near the QRRRW in the catalytic domain caused a rise in the hydrogen bond between UDP-GlcNAc and chitin synthase, and its chitin content was higher than that in the Bis-UNSEL strain. Nevertheless, the sensitivity of the Bis-SEL strain to bistrifluron was significantly recovered when it was knocked down though RNA interference. The fitness advantages of bistrifluron resistance may be related to the up-regulation and mution of chitin sy
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