SUMMARY The ability of plants to reprogram their metabolism in response to fluctuating environments, referred to as metabolic plasticity, is a key feature that enables sessile organisms to maintain growth, survival, and reproduction under changing conditions. As a mechanistic component of phenotypic plasticity, metabolic plasticity can buffer environmental perturbations and confer adaptive advantages. However, despite growing evidence for extensive metabolic remodeling under stress, the genetic and regulatory basis of this plasticity remains incompletely understood. Here, we review metabolic plasticity across major metabolic domains in plants, with emphasis on carbon, nitrogen, photorespiratory, and lipid metabolism, emphasizing how environmental cues and genetic regulation jointly shape metabolic responses. We conclude that, although metabolic plasticity is widespread in plants, its mechanistic and genetic basis remains incompletely understood; population‐scale studies and mathematical modeling offer promising avenues to resolve this gap and extend current insights from model systems to crops.
SUMMARY Perennial plants rely on two key ecological strategies to supply nitrogen (N) for photosynthetic tissue construction: root N remobilization (internal cycling) and soil N uptake. How plants trade‐off these strategies determines the economy of N use and is likely context‐dependent. Yet, it is rarely quantified in situ across growth stages and under varying management, limiting the mechanistic understanding of how plants rebalance N‐use trade‐offs to adapt to grazing disturbance. To address this gap, we conducted an in situ experiment using 15 N isotope labelling techniques in a semiarid grassland to quantify the contributions of these two strategies at two plant growth stages under nil, summer or autumn grazing. We found that the plant relied more on soil N uptake (58%) during the regreen stage, but more on N remobilization (57%) during the rapid‐growth stage. Grazing, especially in autumn, significantly leaned N use trade‐off toward conservative N remobilization. The shift in plant N use strategies was driven primarily by plant growth demand and soil N supply, but not root N stock. Plant N use trade‐off leaned toward internal cycling when source traits were below or sink traits were above the thresholds, for example, soil N availability <9.0 mg kg −1 or shoot carbon content >41.88%. Our study highlights the importance of the N resource‐sink relations in mediating the trade‐off in plant N use strategies, buffering grazing stress to grassland plants. These findings provide a mechanistic basis for improving ecosystem N cycling modeling and adaptive grazing management.
SUMMARY Land plant mitochondria and plastids are endosymbiotic organelles that possess their own, reduced genomes. Gene expression is largely regulated at the transcript level, predominantly by nuclear‐encoded proteins. Notably, up to thousands of cytidines in organellar RNAs are specifically edited to uridines, mostly restoring conserved genetic information. Key players in this process are nuclear‐encoded pentatricopeptide repeat (PPR) proteins, which bind target RNAs in a one‐PPR:one‐nucleotide manner, following a two‐amino‐acid‐based code. Cytidine deamination is catalyzed by intrinsic or trans ‐ acting DYW domains. The modularity and programmability of PPR‐RNA interactions make PPR editing factors attractive candidates for the development of biotechnological tools. However, RNA target selection is not determined by the ‘PPR code’ alone, hampering the generation of highly effective and specific editors. Refining such tools requires efficient assays to dissect the determinants of editor‐RNA interaction. Here, we introduce a rapid assay to assess PPR editor specificity through transient expression in the cytosol of Nicotiana benthamiana , which offers a large and diverse transcriptome that enables extensive off‐target editing. Profiling of these off‐targets provides comprehensive information on an editor's target selectivity. Compared with a previous setup in the model moss Physcomitrium patens , which relies on stable transformation, the required experimental time is reduced from months to days. We demonstrate the power of the system by characterizing the off‐targets of the moss editor PpPPR56. The new assay allows rapid functional assessment of editing factor variants and removes a bottleneck in understanding editor‐RNA interactions, which is a prerequisite for the rational improvement of PPR‐based RNA editing tools.
SUMMARY Population genetic theory predicts that species with narrow geographic distributions experience stronger genetic drift, higher inbreeding, and greater mutational burden than their widespread relatives, yet how demographic history shapes the genomic basis of adaptation remains poorly understood. We hypothesized that (i) restricted‐range species exhibit reduced genetic diversity, elevated inbreeding, and greater mutation load owing to smaller long‐term effective population sizes; (ii) despite these demographic constraints, shared environmental pressures can still drive repeated adaptation; (iii) repeated adaptation may arise through ancestral standing genetic variation, adaptive introgression, or independent de novo mutations. We tested these hypotheses using two kiwifruit species, Actinidia hemsleyana (narrow‐ranged) and Actinidia eriantha (widespread), which differ markedly in demographic history and range size but occupy overlapping environments in subtropical China. We show that demographic contraction and inbreeding have eroded genome‐wide diversity in the range‐restricted species, accompanied by a substantially higher load of deleterious mutations. Despite these contrasting demographic legacies, both species exhibit repeated genomic responses to shared climatic gradients, with adaptation targeting similar genes. Such repeated adaptation was driven primarily by ancestral standing variation, with smaller contributions from adaptive introgression and only limited evidence for independent de novo mutations. These results reveal that demographic constraints shape genome‐wide diversity and mutation load but do not preclude repeated adaptation when shared genetic variation remains available.
SUMMARY SQUAMOSA PROMOTER BINDING PROTEIN‐LIKE 8 (SPL8) is a plant‐specific transcription factor essential for anther development, but its regulatory partners and downstream mechanisms remain largely unknown. We identified 26 SPL8‐interacting transcription factors by yeast two‐hybrid screening and bimolecular fluorescence complementation (BiFC) assays, with YABBY (YAB) and TEOSINTE BRANCHED 1/CYCLOIDEA/PCF (TCP) family emerging as the predominant interactors. Among these, YAB3 and TCP19 were selected for detailed characterization. Their interactions with SPL8, as well as with each other, were confirmed in plant nuclei by fluorescence resonance energy transfer–fluorescence lifetime imaging microscopy (FRET‐FLIM). Chromatin immunoprecipitation sequencing (ChIP‐seq), ChIP‐qPCR, yeast one‐hybrid, and dual‐luciferase assays demonstrated that SPL8 directly binds the regulatory regions of YAB3 and TCP19 and activates their transcription. Dexamethasone‐inducible expression assays further showed that this induction occurs independently of de novo protein synthesis. Expression analyses revealed overlapping spatial and temporal patterns of SPL8 , YAB3 , and TCP19 during early anther development, particularly in tapetal cells, microspore mother cells, and vascular tissues. Genetic and cellular analyses of promoter‐driven SRDX repression lines showed that SPL8 , YAB3 , and TCP19 regulate anther morphogenesis, tapetal differentiation, meiotic progression, and microspore development. Although individual family members exhibited functional redundancy, their repression caused severe developmental defects and male sterility. Together, these findings establish the SPL8 – YAB3 / TCP19 module as a multilayered regulatory system in which SPL8 controls anther development through both transcriptional activation of YAB3 and TCP19 and physical interaction with these proteins, expanding the regulatory framework of SPL ‐mediated reproductive development.
