Conjoined partners: efficacy and side effects of grafting and dsRNA application on the microbial endophyte population of grapevine plants inoculated with two esca-related fungal pathogens.

Grafting has been exploited since 7000 BC to enhance productivity, disease resistance, and adaptability of cultivated plants to stressful conditions especially in woody crops such as grapevine (Vitis spp.). In contrast, the application of sequence specific double-stranded RNAs (dsRNAs) to control fungal pathogens and insect pests has only been recently developed.

Increased nuclear import characterizes aberrant nucleocytoplasmic transport in neurons from patients with spinocerebellar ataxia type 7.

Introduction: Spinocerebellar ataxia type 7 (SCA7) is an inherited neurodegenerative disorder characterized by cerebellar and retinal degeneration. SCA7 is caused by a CAG-polyglutamine repeat expansion in the ataxin-7 gene, which encodes a transcription factor protein that is a core component of the STAGA co-activator complex. As ataxin-7 protein regularly shuttles between the nucleus and the cytosol, we sought to test if polyglutamine-expanded ataxin-7 protein results in nuclear membrane abnormalities or defects in nucleocytoplasmic (N/C) transport.

CRISPR/Cas9-driven double modification of grapevine MLO6-7 imparts powdery mildew resistance, while editing of NPR3 augments powdery and downy mildew tolerance.

The implementation of genome editing strategies in grapevine is the easiest way to improve sustainability and resilience while preserving the original genotype. Among others, the Mildew Locus-O (MLO) genes have already been reported as good candidates to develop powdery mildew-immune plants. A never-explored grapevine target is NPR3, a negative regulator of the systemic acquired resistance.

Dysregulation of zebrin-II cell subtypes in the cerebellum is a shared feature across polyglutamine ataxia mouse models and patients.

Spinocerebellar ataxia type 7 (SCA7) is a genetic neurodegenerative disorder caused by a CAG-polyglutamine repeat expansion. Purkinje cells (PCs) are central to the pathology of ataxias, but their low abundance in the cerebellum underrepresents their transcriptomes in sequencing assays. To address this issue, we developed a PC enrichment protocol and sequenced individual nuclei from mice and patients with SCA7.