Marker and readout genes for defense priming in Pseudomonas cannabina pv. alisalensis interaction aid understanding systemic immunity in Arabidopsis.

Following localized infection, the entire plant foliage becomes primed for enhanced defense. However, specific genes induced during defense priming (priming-marker genes) and those showing increased expression in defense-primed plants upon rechallenge (priming-readout genes) remain largely unknown. In our Arabidopsis thaliana study, genes AT1G76960 (function unknown), CAX3 (encoding a vacuolar Ca2+/H+ antiporter), and CRK4 (encoding a cysteine-rich receptor-like protein kinase) were strongly expressed during Pseudomonas cannabina pv. alisalensis-induced defense priming, uniquely marking the primed state for enhanced defense. Conversely, PR1 (encoding a pathogenesis-related protein), RLP23 and RLP41 (both encoding receptor-like proteins) were similarly activated in defense-primed plants before and after rechallenge, suggesting they are additional marker genes for defense priming. In contrast, CASPL4D1 (encoding Casparian strip domain-like protein 4D1), FRK1 (encoding flg22-induced receptor-like kinase), and AT3G28510 (encoding a P loop-containing nucleoside triphosphate hydrolases superfamily protein) showed minimal activation in uninfected, defense-primed, or rechallenged plants, but intensified in defense-primed plants after rechallenge. Notably, mutation in only priming-readout gene NHL25 (encoding NDR1/HIN1-like protein 25) impaired both defense priming and systemic acquired resistance, highlighting its previously undiscovered pivotal role in systemic plant immunity.

Task-based profiles of language impairment and their relationship to cognitive dysfunction in Parkinson's disease.

OBJECTIVE: Parkinson's Disease (PD) is associated with both motor and non-motor problems, such as cognitive impairment. Particular focus in this area has been on the relationship between language impairment and decline in other cognitive functions, with the literature currently inconclusive on how the nature and degree of language impairment relate to cognition or other measures of disease severity. In addition, little information is available on how language problems identified in experimental task set-ups relate to competency in self-generated language paradigms such as picture description, monologues or conversations. This study aimed to inform clinical management of language impairment in PD by exploring (1) language performance across a range of experimental as well as self-generated language tasks, (2) how the relationship between these two aspects might be affected by the nature of the cognitive and language assessment; and (3) to what degree performance can be predicted across the language tasks. METHODS: 22 non-demented people with PD (PwPD) and 22 healthy control participants performed a range of cognitive and language tasks. Cognitive tasks included a screening assessment in addition to tests for set shifting, short term memory, attention, as well as letter and category fluency. Language was investigated in highly controlled grammar tasks as well as a Sentence Generation and a Narrative. RESULTS: The study highlighted impaired ability in set-shifting and letter fluency in the executive function tasks, and a higher rate of grammatical and lexical errors across all language tasks in the PD group. The performance in the grammar task was linked to set shifting ability, but error rates in Sentence Generation and Narrative were independent of this. There was no relevant relationship between performances across the three language tasks. CONCLUSIONS: Our results suggest that there is a link between executive function and language performance, but that this is task dependent in non-demented PwPD. This has implications for the management of language impairment in PD, both for assessment and for designing effective interventions.