Phase separation of S-RNase promotes self-incompatibility in Petunia hybrida

Self-incompatibility(SI)is an intraspecific reproductive barrier widely present in angiosperms.The SI system with the broadest occurrence in angiosperms is based on an S-RNase linked to a cluster of multiple S-locus F-box(SLF)genes found in the Solanaceae,Plantaginaceae,Rosaceae,and Rutaceae.Recent studies reveal that non-self S-RNase is degraded by the Skip Cullin F-box(SCF)SLF-mediated ubiquitin–proteasome system in a collaborative manner in Petunia,but how self-RNase functions largely remains mysterious.Here,we show that S-RNases form S-RNase condensates(SRCs)in the self-pollen tube cytoplasm through phase separation and the disruption of SRC formation breaks SI in self-incompatible Petunia hybrida.We further find that the pistil SI factors of a small asparagine-rich protein HT-B and thioredoxin h together with a reduced state of the pollen tube all promote the expansion of SRCs,which then sequester several actin-binding proteins,including the actin polymerization factor PhABRACL,the actin polymerization activity of which is reduced by S-RNase in vitro.Meanwhile,we find that S-RNase variants lacking condensation ability fail to recruit PhABRACL and are unable to induce actin foci formation required for pollen tube growth inhibition.Taken together,our results demonstrate that phase separation of S-RNase promotes SI response in P.hybrida,revealing a new mode of S-RNase action.

Correction to:Rescue of premature aging defects in Cockayne syndrome stem cells by CRISPR/Cas9-mediated gene correction

CORRECTION TO:PROTEIN CELL HTTPS://DOI.ORG/10.1007/S13238-019-0623-2 In Fig.7C,we used the ERCC6mut.iPSCs(CS iPSCs)as NANOG positive control pluripotent cells in the upper pan-els.However,these cells were inadvertently labeled as ERCC6^(GC)-iPSCs.In the revised version of Fig.7C,we have updated the high-quality images along with the corrected mark.In addition,we have also made corresponding chan-ges in the figure legend.

SIRT7 antagonizes human stem cell aging as a heterochromatin stabilizer

SIRT7,a sirtuin family member implicated in aging and disease,is a regulator of metabolism and stress responses.It remains elusive how human somatic stem cell populations might be impacted by SIRT7.Here,we found that SIRT7 expression declines during human mesenchymal stem cell(hMSC)aging and that SIRT7 deficiency accelerates senescence.Mechanistically,SIRT7 forms a complex with nuclear lamina proteins and heterochromatin proteins,thus maintaining the repressive state of heterochromatin at nuclear periphery.Accordingly,deficiency of SIRT7 results in loss of heterochromatin,derepression of the LINE1 retrotransposon(LINE1),and activation of innate immune signaling via the cGAS-STING pathway.These agingassociated cellular defects were reversed by overexpression of heterochromatin proteins or treatment with a LINE1 targeted reverse-transcriptase inhibitor.Together,these findings highlight how SIRT7 safeguards chromatin architecture to control innate immune regulation and ensure geroprotection during stem cell aging.