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A barley powdery mildew fungus non-autonomous retrotransposon encodes a peptide that supports penetration success on barley

机译:大麦白粉病真菌非自主逆转录转座子编码支持大麦穿透成功的肽

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摘要

Pathogens overcome plant immunity by means of secreted effectors. Host effector targets often act in pathogen defense, but might also support fungal accommodation or nutrition. The barley ROP GTPase HvRACB is involved in accommodation of fungal haustoria of the powdery mildew fungus Blumeria graminis f.sp. hordei (Bgh) in barley epidermal cells. We found that HvRACB interacts with the ROP-interactive peptide 1 (ROPIP1) that is encoded on the active non-long terminal repeat retroelement Eg-R1 of Bgh. Overexpression of ROPIP1 in barley epidermal cells and host-induced post-transcriptional gene silencing (HIGS) of ROPIP1 suggested that ROPIP1 is involved in virulence of Bgh. Bimolecular fluorescence complementation and co-localization supported that ROPIP1 can interact with activated HvRACB in planta. We show that ROPIP1 is expressed by Bgh on barley and translocated into the cytoplasm of infected barley cells. ROPIP1 is recruited to microtubules upon co-expression of MICROTUBULE ASSOCIATED ROP GTPase ACTIVATING PROTEIN (HvMAGAP1) and can destabilize cortical microtubules. The data suggest that Bgh ROPIP targets HvRACB and manipulates host cell microtubule organization for facilitated host cell entry. This points to a possible neo-functionalization of retroelement-derived transcripts for the evolution of a pathogen virulence effector.
机译:病原体通过分泌的效应子克服了植物的免疫力。宿主效应子靶通常在病原体防御中起作用,但也可能支持真菌调节或营养。大麦ROP GTPase HvRACB参与白粉病真菌Blumeria graminis f.sp.大麦表皮细胞中的hordei(Bgh)。我们发现HvRACB与Bgh的活性非长末端重复元件Eg-R1上编码的ROP相互作用肽1(ROPIP1)相互作用。大麦表皮细胞中ROPIP1的过表达和宿主诱导的ROPIP1转录后基因沉默(HIGS)表明ROPIP1参与了Bgh的毒力。双分子荧光互补和共定位支持ROPIP1可以与植物体内活化的HvRACB相互作用。我们显示ROPIP1由Bgh在大麦上表达,并转移到被感染大麦细胞的细胞质中。在微管相关的ROP GTPase活化蛋白(HvMAGAP1)的共表达下,ROPIP1被募集到微管中,并且可以使皮层微管不稳定。数据表明Bgh ROPIP靶向HvRACB并操纵宿主细胞微管组织,以促进宿主细胞进入。这指出了可能由新的逆向功能转录本功能化,用于病原体毒力效应子的进化。

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