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Plant nucleotide-binding leucine-rich repeat receptors (NLRs) regulate immunity and cell death. InArabidopsis, a subfamily of “helper” NLRs is required by many “sensor” NLRs. Active NRG1.1 oligomerized, was enriched in plasma membrane puncta, and conferred cytoplasmic calcium ion (Ca2+) influx in plant and human cells. NRG1.1-dependent Ca2+influx and cell death were sensitive to Ca2+channel blockers and were suppressed by mutations affecting oligomerization or plasma membrane enrichment. Ca2+influx and cell death mediated by NRG1.1 and ACTIVATED DISEASE RESISTANCE 1 (ADR1), another helper NLR, required conserved negatively charged N-terminal residues. Whole-cell voltage-clamp recordings demonstrated thatArabidopsishelper NLRs form Ca2+-permeable cation channels to directly regulate cytoplasmic Ca2+levels and consequent cell death. Thus, helper NLRs transduce cell death signals directly.
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This content will become publicly available on February 14, 2026
Distinct input-specific mechanisms enable presynaptic homeostatic plasticity
Synapses are endowed with the flexibility to change through experience, but must be sufficiently stable to last a lifetime. This tension is illustrated at theDrosophilaneuromuscular junction (NMJ), where two motor inputs that differ in structural and functional properties coinnervate most muscles to coordinate locomotion. To stabilize NMJ activity, motor neurons augment neurotransmitter release following diminished postsynaptic glutamate receptor functionality, termed presynaptic homeostatic potentiation (PHP). How these distinct inputs contribute to PHP plasticity remains enigmatic. We have used a botulinum neurotoxin to selectively silence each input and resolve their roles in PHP, demonstrating that PHP is input specific: Chronic (genetic) PHP selectively targets the tonic MN-Ib, where active zone remodeling enhances Ca2+influx to promote increased glutamate release. In contrast, acute (pharmacological) PHP selectively increases vesicle pools to potentiate phasic MN-Is. Thus, distinct homeostatic modulations in active zone nanoarchitecture, vesicle pools, and Ca2+influx collaborate to enable input-specific PHP expression.
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- Award ID(s):
- 2417451
- PAR ID:
- 10620855
- Publisher / Repository:
- Science
- Date Published:
- Journal Name:
- Science Advances
- Volume:
- 11
- Issue:
- 7
- ISSN:
- 2375-2548
- Format(s):
- Medium: X
- Sponsoring Org:
- National Science Foundation
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