nk92 effector cells  (ATCC)

Journal: Horticulture Research

Article Title: Solanaceous vegetables and Fusarium oxysporum interactions: pathogen genomics, pathogenesis, host resistance, and emerging microbiome-driven disease management

doi: 10.1093/hr/uhag074

Figure Lengend Snippet: Regulatory mechanisms controlling effector gene expression during Fol infection. Transcription of effector genes is controlled by chromatin modification and a network of transcription factors. During the early infection stage, increased levels of histone acetyltransferase FolSas2 undergoes autoacetylation at lysine 269, which prevents its 26S proteasome-mediated degradation and enables histone H4K8 hyperacetylation, promoting transcription of effector genes. At other stages, elevated FolSir1 deacetylates FolSas2, promoting FolSas2 degradation. The WOPR-domain-containing transcription factor Sge1 directly activates SIX and other effector genes, and the pathogenicity chromosome-encoded FTF1, a homolog of Sge1, enhances effector gene expression in an Sge1-dependent manner during infection. Its core-chromosome homolog FTF2 also induces effector gene expression by binding to their promoters.

Article Snippet: For example, several known Secreted In Xylem (SIX) effector genes, including SIX7 , SIX8 , SIX11 , SIX12 , and SIX14 , were not originally annotated in the Fol 4287 genome, while SIX10 possesses annotation errors, which hinders the comprehensive identification of novel effectors, thereby limiting insights into the molecular basis of Fol virulence [ ].

Techniques: Gene Expression, Infection, Modification, Binding Assay