Lucia Marti

TL;DR: It is established that the aberrant phenotype was due to a missense recessive mutation in sec24A, one of the three Arabidopsis isoforms encoding the coat protomer complex II (COPII) protein Sec24, and that the mutation affects the distribution of this critical component at ER export sites.

TL;DR: It is shown how antiviral inhibitors bind to portions of α-GluII that are unique to this enzyme, and this opens the way to the development of potent and selective antivirals against existing and emerging infectious disease.

TL;DR: It is shown that AtLYK3 also negatively regulates basal expression of defense genes and resistance to Botrytis cinerea and Pectobacterium carotovorum infection and is important for the cross talk between signaling pathways activated by ABA and pathogens.

TL;DR: This review addresses the most recent advances in the distribution and regulation of ER-to-Golgi protein transport intermediates and functional analyses of COPII isoforms and new studies support that such isoforms might not be functionally redundant and that they might have unanticipated roles in maintaining the integrity of the ER.

TL;DR: Findings point to ANPs as key transduction elements that coordinate damage- and pathogen-associated molecular pattern-triggered immunity and orchestrate reactive oxygen species accumulation and signaling.