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https://www.selleckchem.com/products/midostaurin-pkc412.html Plants have a variety of strategies to avoid canopy shade and compete with their neighbors for light, collectively called the shade avoidance syndrome (SAS). Plants also have extensive systems to defend themselves against pathogens and herbivores. Defense and shade avoidance are two fundamental components of plant survival and productivity, and there are often tradeoffs between growth and defense. Recently, MYC2, a major positive regulator of defense, was reported to inhibit elongation during shade avoidance. Here, we further investigate the role of MYC2 and the related MYC3 and MYC4 in shade avoidance, and we examine the relationship between MYC2/3/4 and the PIF family of light-regulated transcription factors. We demonstrate that MYC2/3/4 inhibit both elongation and flowering. Furthermore, using both genetic and transcriptomic analysis we find that MYCs and PIFs generally function independently in growth regulation. However, surprisingly, the pif4/5/7 triple mutant restored the petiole shade avoidance response of myc2 (jin1-2) and myc2/3/4 We theorize that increased petiole elongation in myc2/3/4 could be more due to resource tradeoffs or post-translational modifications rather than interactions with PIF4/5/7 affecting gene regulation. Copyright © The Author(s) 2020. Published by the Genetics Society of America.DNA can assemble into non-B form structures that stall replication and cause genomic instability. One such secondary structure results from an inverted DNA repeat that can assemble into hairpin and cruciform structures during DNA replication. Quasipalindromes (QP), imperfect inverted repeats, are sites of mutational hotspots. Quasipalindrome-associated mutations (QPMs) occur through a template-switch mechanism in which the replicative polymerase stalls at a QP site and uses the nascent strand as a template instead of the correct template strand. This mutational event causes the QP to become a perfe

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