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Abstract Fragmentation transforms the environment along forest edges. The prevailing narrative, driven by research in tropical systems, suggests that edge environments increase tree mortality and structural degradation resulting in net decreases in ecosystem productivity. We show that, in contrast to tropical systems, temperate forest edges exhibit increased forest growth and biomass with no change in total mortality relative to the forest interior. We analyze >48,000 forest inventory plots across the north-eastern US using a quasi-experimental matching design. At forest edges adjacent to anthropogenic land covers, we report increases of 36.3% and 24.1% in forest growth and biomass, respectively. Inclusion of edge impacts increases estimates of forest productivity by up to 23% in agriculture-dominated areas, 15% in the metropolitan coast, and +2% in the least-fragmented regions. We also quantify forest fragmentation globally, at 30-m resolution, showing that temperate forests contain 52% more edge forest area than tropical forests. Our analyses upend the conventional wisdom of forest edges as less productive than intact forest and call for a reassessment of the conservation value of forest fragments. 

Commitment to cell division at the end of G1 phase, termed Start in the budding yeast Saccharomyces cerevisiae , is strongly influenced by nutrient availability. To identify new dominant activators of Start that might operate under different nutrient conditions, we screened a genome-wide ORF overexpression library for genes that bypass a Start arrest caused by absence of the G1 cyclin Cln3 and the transcriptional activator Bck2. We recovered a hypothetical gene YLR053c , renamed NRS1 for Nitrogen-Responsive Start regulator 1, which encodes a poorly characterized 108 amino acid microprotein. Endogenous Nrs1 was nuclear-localized, restricted to poor nitrogen conditions, induced upon TORC1 inhibition, and cell cycle-regulated with a peak at Start. NRS1 interacted genetically with SWI4 and SWI6 , which encode subunits of the main G1/S transcription factor complex SBF. Correspondingly, Nrs1 physically interacted with Swi4 and Swi6 and was localized to G1/S promoter DNA. Nrs1 exhibited inherent transactivation activity, and fusion of Nrs1 to the SBF inhibitor Whi5 was sufficient to suppress other Start defects. Nrs1 appears to be a recently evolved microprotein that rewires the G1/S transcriptional machinery under poor nitrogen conditions.