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Abstract Nitrogen (N) doped graphene materials have been synthesized using the sole precursor adenine on the Ir(111) and Ru(0001) surfaces. X-ray photoelectron spectroscopy and scanning tunneling microscopy (STM) have been used to characterize the obtained N-doped graphene materials. Several graphitic and pyridinic N dopants have been identified on the atomic scale by combining STM measurements and STM simulations based on density functional theory calculations. 

SUMMARY Plastid‐to‐nucleus communication, crucial for regulating stress‐responsive gene expression, has long intrigued researchers. This study reveals how the plastidial metabolite 2‐C‐methyl‐D‐erythritol‐2,4‐cyclopyrophosphate (MEcPP) orchestrates transcriptional reprogramming by modulating the rapid stress response element (RSRE), a conserved regulatory hub in the plant general stress response network. Yeast one‐hybrid assays identified HAT1, a class II HD‐Zip protein, as a negative regulator of RSRE. Genetic analyses, including HAT1 overexpression and knockdowns, confirmed its role in suppressing RSRE activity. Interaction assays uncovered a suppression network involving HAT1, the co‐repressor TOPLESS (TPL), and the nuclear importin IMPα‐9. Furthermore, HAT1 interacts with calmodulin‐binding transcription activator 3 (CAMTA3), a calcium/calmodulin‐binding transcription factor known to activate RSRE. AlphaFold modeling provided insights into the architecture of the HAT1‐RSRE complex and HAT‐CAMTA3 interaction, supported by conserved domains across plant species. Under stress condition, MEcPP accumulation promotes the 26S proteasomal degradation of TPL and IMPα‐9 while reduces auxin‐dependent HAT1 expression. Additionally, MEcPP enhances Ca²⁺influx, activating CAMTA3 and enabling it to bind RSRE, thereby initiating the transcription of stress response genes. This dual mechanism—dismantling suppressors (HAT1, TPL, and IMPα‐9) and activating CAMTA3—underscores MEcPP's central role in plastid‐to‐nucleus signaling. These findings emphasize MEcPP's pivotal function in dynamically regulating gene expression to maintain cellular homeostasis under environmental stress. 

Tree growth and longevity trade-offs fundamentally shape the terrestrial carbon balance. Yet, we lack a unified understanding of how such trade-offs vary across the world’s forests. By mapping life history traits for a wide range of species across the Americas, we reveal considerable variation in life expectancies from 10 centimeters in diameter (ranging from 1.3 to 3195 years) and show that the pace of life for trees can be accurately classified into four demographic functional types. We found emergent patterns in the strength of trade-offs between growth and longevity across a temperature gradient. Furthermore, we show that the diversity of life history traits varies predictably across forest biomes, giving rise to a positive relationship between trait diversity and productivity. Our pan-latitudinal assessment provides new insights into the demographic mechanisms that govern the carbon turnover rate across forest biomes.