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. 2022 Sep 9;23(18):10445. doi: 10.3390/ijms231810445

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© 2022 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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The expression of FgCSN12-GFP failed to rescue the defects of the Fgcsn12 mutant in ascosporogenesis. (A) Three-day-old PDA cultures of the wild type (PH-1), Fgcsn12 mutant (M11), Fgcsn12/FgCSN12-GFP transformant (CG1), and Fgcsn12/FgCSN12^UTR transformant (CU3). (B) Conidial morphology of the same set of strains. Bar = 10 μm. (C) Mating cultures of the same set of strains were examined at 8 dpf. Arrows point to cirrhi. Bar = 1 mm. (D) Ascospore discharge was assayed with 7 dpf perithecia of the same set of strains. (E) The same set of strains was examined for asci and ascospores in 8 dpf perithecia. Nor, Int, and Mut represent normal, intermediate, and mutant ascospores from transformant CG1, respectively. Bar = 20 μm.