COG7 links Golgi integrity to stress signaling and senescence

The mechanisms linking Golgi function to stress adaptation and senescence remain poorly understood. Here, we identify the conserved oligomeric Golgi (COG) subunit COG7 as a non-redundant determinant of Golgi integrity and stress adaptation in Arabidopsis thaliana. Functional disruption of COG7 reduces Golgi size, enhances Rapid Stress Response Element (RSRE)-dependent stress signaling, and accelerates dark-induced senescence. Complementation analyses reveal functional specialization within the COG complex, as only COG3, COG5, and COG6 partially restore stress signaling and senescence phenotypes. At the molecular level, cog7 exhibits altered glycosylation, increased ubiquitination, and elevated autophagy. However, disruption of glycosylation pathways or dark-induced candidate glycosyltransferases does not affect RSRE activation, proteostasis-associated responses, or senescence progression, indicating that glycosylation changes are downstream consequences rather than drivers of the stress phenotype. Similarly, CAMTA3-dependent RSRE activation is genetically separable from senescence and proteostasis pathways. Together, these findings show that Golgi dysfunction generates multiple parallel outputs rather than a single linear stress pathway and establish COG7 as a central regulator linking Golgi integrity to stress signaling, proteostasis, and senescence during dark-induced stress.