The <i>SGE1</i> Homolog of <i>Fusarium oxysporum</i> f. sp. <i>rapae</i> Is a Pathogenicity Factor and Required for Full Stress Resistance of Chlamydospores

Four <i>Fusarium oxysporum</i> formae speciales can cause yellows disease of the economically important species in Brassicaceae family. Among these, <i>F. oxysporum</i> f. sp. <i>rapae</i> induces yellows in leaf mustard and Chinese cabbage. <i>SGE1</i> (SIX gene expression 1) is a transcription factor characterized by the presence of the WOPR box domain. Homologs of <i>SGE1</i> in other <i>Fusarium</i> species play a crucial role in virulence and regulate the expression of SIX (secreted-in-xylem) effector genes. However, the role of the <i>SGE1</i> homolog in <i>F. oxysporum</i> f. sp. <i>rapae</i> (<i>FoRP-SGE1</i>) in pathogenesis and fungal development remains unexplored. To investigate its function in regulating pathogenicity and fungal development, gene knockout mutants of <i>FoRP-SGE1</i> (Δ<i>FoRP-SGE1</i>) were generated and validated. Δ<i>FoRP-SGE1</i> showed a reduction in conidiation, but normal colony growth and conidial germination. Notably, Δ<i>FoRP-SGE1</i> completely lost pathogenicity, but it retained the ability to colonize leaf mustard plants, indicating that <i>FoRP-SGE1</i> is a key pathogenicity factor. Expression of <i>SIX9</i> and <i>SIX14</i> was significantly diminished in Δ<i>FoRP-SGE1</i>. Furthermore, most chlamydospores of Δ<i>FoRP-SGE1</i> lacked the outermost fibrillose coat. Germination of Δ<i>FoRP-SGE1</i> chlamydospores was also impaired under various stress conditions, including osmotic stress, drought, UV exposure, and fluazinam toxicity. This study presents, for the first time, the role of a <i>Fusarium</i> <i>SGE1</i> homolog in the morphology and persistence of chlamydospores. Collectively, our findings suggest that <i>FoRP-SGE1</i> is a critical pathogenicity factor in the leaf mustard-<i>F. oxysporum</i> f. sp. <i>rapae</i> pathosystem and is involved in the development of the fibrillose coat of chlamydospores and their resistance to environmental stresses.