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Abstract Shade-intolerant plants rapidly elongate their stems, branches, and leaf stalks to compete with neighboring vegetation, maximizing sunlight capture for photosynthesis. This rapid growth adaptation, known as the shade-avoidance response (SAR), comes at a cost: reduced biomass, crop yield, and root growth. Significant progress has been made on the mechanistic understanding of hypocotyl elongation during SAR; however, the molecular interpretation of root growth repression is not well understood. Here, we explore the mechanisms by which SAR induced by low red:far-red light restricts primary and lateral root (LR) growth. By analyzing the whole-genome transcriptome, we identified a core set of shade-induced genes in roots of Arabidopsis (Arabidopsis thaliana) and tomato (Solanum lycopersicum) seedlings grown in the shade. Abiotic and biotic stressors also induce many of these shade-induced genes and are predominantly regulated by WRKY transcription factors. Correspondingly, a majority of WRKY genes were among the shade-induced genes. Functional analysis using transgenics of these shade-induced WRKYs revealed that their role is essentially to restrict primary root and LR growth in the shade; captivatingly, they did not affect hypocotyl elongation. Similarly, we also found that ethylene hormone signaling is necessary for limiting root growth in the shade. We propose that during SAR, shade-induced WRKY26, 45, and 75, and ethylene reprogram gene expression in the root to restrict its growth and development. 

Abstract Oligodendrocyte precursor cells (OPCs) give rise to myelinating oligodendrocytes throughout life, but the functions of OPCs are not limited to oligodendrogenesis. Here we show that OPCs contribute to thalamocortical presynapse elimination in the developing and adult mouse visual cortex. OPC-mediated synapse engulfment increases in response to sensory experience during neural circuit refinement. Our data suggest that OPCs may regulate synaptic connectivity in the brain independently of oligodendrogenesis.