Sclerotinia sclerotiorum causes white mold disease on a wide range of economically important crops such as soybean, canola, tomato, pea and sunflower. As one of the most successful plant pathogens, S. sclerotiorum has the unique ability of adapting to various environmental conditions and effectively suppressing or evading plant defense. Notably, S. sclerotiorum secretes an array of plant cell-wall degrading
enzymes (CWDEs) to macerate host cell wall and utilizes the liberated
monosaccharides and
oligosaccharides as nutrients. One of the major plant cell wall constituents is
polygalacturonic acid in
pectin, with
D-galacturonic acid being the most abundant component. In this research, we identified four S. sclerotiorum genes that encode the
enzymes for the
D-galacturonic acid catabolism, namely Ssgar1, Ssgar2, Sslgd1 and Sslga1. Gene-knockout mutants were created for all four catabolic genes. When cultured on
pectin as the alternative
carbon source, Sslgd1- and Sslga1-deletion mutants and Ssgar1/Ssgar2 double deletion mutants exhibited significantly reduced growth. The
D-galacturonic acid catabolic genes are transcriptionally induced by either
polygalacturonic acid in the
culture media or during host
infection. Virulence tests of the knockout mutants revealed that Ssgar2, Sslgd1 and Sslga1 all facilitated the effective colonization of S. sclerotiorum to the leaves of soybean and pea, but not of tomato which has the lowest
D-galacturonic acid contents in its leaves. In addition to their positive roles in virulence, all four
enzymes negatively affect S. sclerotiorum tolerance to salt stress. SsGAR2 has an additional function in tolerance to
Congo Red, suggesting a potential role in cell wall stability of S. sclerotiorum. This study is the first report revealing the versatile functions of
D-galacturonic acid catabolic genes in S. sclerotiorum virulence, salinity response and cell wall integrity.