Fusarium graminearum effector FgEC1 targets wheat TaGF14b protein to suppress TaRBOHD-mediated ROS production and promote infection

Fusarium head blight(FHB), caused by Fusarium graminearum, is a devastating disease of wheat globally. However, the molecular mechanisms underlying the interactions between F. graminearum and wheat remain unclear. Here, we identified a secreted effector protein, FgEC1, that is induced during wheat infection and is required for F. graminearum virulence. FgEC1 suppressed flg22-and chitin-induced callose deposition and reactive oxygen species(ROS) burst in Nicotiana benthamiana. FgEC1 directly interacts with TaGF14b, which is upregulated in wheat heads during F. graminearum infection. Overexpression of TaGF14b increases FHB resistance in wheat without compromising yield. TaGF14b interacts with NADPH oxidase respiratory burst oxidase homolog D(TaRBOHD) and protects it against degradation by the 26S proteasome. FgEC1 inhibited the interaction of TaGF14b with TaRBOHD and promoted TaRBOHD degradation, thereby reducing TaRBOHD-mediated ROS production.Our findings reveal a novel pathogenic mechanism in which a fungal pathogen acts via an effector to reduce TaRBOHD-mediated ROS production.

FHA2 is a plant-specific ISWI subunit responsible for stamen development and plant fertility^FA

Imitation Switch(ISWI)chromatin remodelers are known to function in diverse multi-subunit complexes in yeast and animals.However,the constitution and function of ISWI complexes in Arabidopsis thaliana remain unclear.In this study,we identified forkheadassociated domain 2(FHA2)as a plant-specific subunit of an ISWI chromatin-remodeling complex in Arabidopsis.By in vivo and in vitro analyses,we demonstrated that FHA2 directly binds to RLT1 and RLT2,two redundant subunits of the ISWI complex in Arabidopsis.The stamen filament is shorter in the fha2 and rlti/2 mutants than in the wild type,whereas their pistil lengths are comparable.The shorter filament,which is due to reduced cell size,results in insufficient pollination and reduced fertility.The rlt1/2 mutant shows an early-floweringphenotype,whereas the phenotype is not shared bythe fha2 mutant.Consistent with the functional specif-icity of FHA2,our RNA-seq analysis indicated that thefha2 mutant affects a subset of RLT1/2-regulated genesthat does not include genes involved in the regulation offlowering time.This study demonstrates that FHA2functions as a previously uncharacterized subunit of theArabidopsis ISwI complex and is exclusively involved inregulating stamen development and plant fertility.

A domesticated Harbinger transposase forms a complex with HDA6 and promotes histone H3 deacetylation at genes but not TEs in Arabidopsis

In eukaryotes,histone acetylation is a major modification on histone N-terminal tails that is tightly connected to transcriptional activation.HDA6 is a histone deacetylase involved in the transcriptional regulation of genes and transposable elements(TEs)in Arabidopsis thaliana.HDA6 has been shown to participate in several complexes in plants,including a conserved SIN3 complex.Here,we uncover a novel protein complex containing HDA6,several Harbinger transposon-derived proteins(HHP1,SANT1,SANT2,SANT3,and SANT4),and MBD domain-containing proteins(MBD1,MBD2,and MBD4).We show that mutations of all four SANT genes in the sant-null mutant cause increased expression of the flowering repressors FLC,MAF4,and MAF5,resulting in a late flowering phenotype.Transcriptome deep sequencing reveals that while the SANT proteins and HDA6 regulate the expression of largely overlapping sets of genes,TE silencing is unaffected in sant-null mutants.Our global histone H3 acetylation profiling shows that SANT proteins and HDA6 modulate gene expression through deacetylation.Collectively,our findings suggest that Harbinger transposon-derived SANT domain-containing proteins are required for histone deacetylation and flowering time control in plants.