In this study, we investigated to possible role of Ras2 in Fusarium circinatum- a fungus that causes pine pitch canker disease on many different pine species and has a wide geographic distribution. This protein is encoded by the RAS2 gene and has been shown to control growth and pathogenicity in a number of fungi in a mitogen-activated protein kinase- and/or cyclic adenosyl monophosphate pathway-dependent manner. The aim was therefore to characterize the phenotypes of RAS2 gene knockout and complementation mutants of F. circinatum. These mutants were generated by transforming protoplasts of the fungus with suitable split-marker constructs. The mutant strains, together with the wild type strain, were used in growth studies as well as pathogenicity assays on Pinus patula seedlings. Results showed that the knockout mutant strain produced significantly smaller lesions compared to the complementation mutant and wild type strains. Growth studies also showed significantly smaller colonies and delayed conidial germination in the knockout mutant strain compared to the complement mutant and wild type strains. Interestingly, the knockout mutant strain produced more macroconidia than the wild type strain. Collectively, these results showed that Ras2 plays an important role in both growth and pathogenicity of F. circinatum. Future studies will seek to determine the pathway(s) through which Ras2 controls these traits in F. circinatum.

在这项研究中，我们调查了 Ras2 在Fusarium circinatum 中的可能作用- Fusarium circinatum - 一种在许多不同松树物种上引起松树沥青溃疡病的真菌，并且具有广泛的地理分布。该蛋白质由RAS2基因编码，并已显示以丝裂原活化蛋白激酶和/或环腺苷单磷酸途径依赖性方式控制许多真菌的生长和致病性。因此，目的是表征F. circinatum的RAS2基因敲除和互补突变体的表型. 这些突变体是通过用合适的分裂标记构建体转化真菌的原生质体而产生的。突变菌株与野生型菌株一起用于生长研究以及对松树幼苗的致病性测定。结果表明，与互补突变体和野生型菌株相比，敲除突变株产生的损伤明显更小。生长研究还表明，与补体突变体和野生型菌株相比，敲除突变菌株的菌落明显更小，分生孢子萌发延迟。有趣的是，敲除突变株比野生型株产生更多的大分生孢子。总的来说，这些结果表明 Ras2 在F. circinatum 的生长和致病性中起着重要作用. 未来的研究将寻求确定 Ras2 在F. circinatum 中控制这些性状的途径。