It is time to move: Heat-induced translocation events.

Climate change-induced temperature fluctuations impact agricultural productivity through short-term intense heat waves or long-term heat stress. Plants have evolved sophisticated strategies to deal with heat stress. Understanding perception and transduction of heat signals from outside to inside cells is essential to improve plant thermotolerance. In this review, we will focus on translocation of molecules and proteins associated with signal transduction to understand how plant cells decode signals from the environment to trigger a suitable response.

Using quantitative methods to understand leaf epidermal development.

As the interface between plants and the environment, the leaf epidermis provides the first layer of protection against drought, ultraviolet light, and pathogen attack. This cell layer comprises highly coordinated and specialised cells such as stomata, pavement cells and trichomes. While much has been learned from the genetic dissection of stomatal, trichome and pavement cell formation, emerging methods in quantitative measurements that monitor cellular or tissue dynamics will allow us to further investigate cell state transitions and fate determination in leaf epidermal development. In this review, we introduce the formation of epidermal cell types in Arabidopsis and provide examples of quantitative tools to describe phenotypes in leaf research. We further focus on cellular factors involved in triggering cell fates and their quantitative measurements in mechanistic studies and biological patterning. A comprehensive understanding of how a functional leaf epidermis develops will advance the breeding of crops with improved stress tolerance.

Misregulation of MYB16 expression causes stomatal cluster formation by disrupting polarity during asymmetric cell divisions.

Stomatal pores and the leaf cuticle regulate evaporation from the plant body and balance the tradeoff between photosynthesis and water loss. MYB16, encoding a transcription factor involved in cutin biosynthesis, is expressed in stomatal lineage ground cells, suggesting a link between cutin biosynthesis and stomatal development. Here, we show that the downregulation of MYB16 in meristemoids is directly mediated by the stomatal master transcription factor SPEECHLESS (SPCH) in Arabidopsis thaliana. The suppression of MYB16 before an asymmetric division is crucial for stomatal patterning, as its overexpression or ectopic expression in meristemoids increased stomatal density and resulted in the formation of stomatal clusters, as well as affecting the outer cell wall structure. Expressing a cutinase gene in plants ectopically expressing MYB16 reduced stomatal clustering, suggesting that cutin affects stomatal signaling or the polarity setup in asymmetrically dividing cells. The clustered stomatal phenotype was rescued by overexpressing EPIDERMAL PATTERNING FACTOR2, suggesting that stomatal signaling was still functional in these plants. Growing seedlings ectopically expressing MYB16 on high-percentage agar plates to modulate tensile strength rescued the polarity and stomatal cluster defects of these seedlings. Therefore, the inhibition of MYB16 expression by SPCH in the early stomatal lineage is required to correctly place the polarity protein needed for stomatal patterning during leaf morphogenesis.

Correction: FIN219/JAR1 and cryptochrome1 antagonize each other to modulate photomorphogenesis under blue light in Arabidopsis.

[This corrects the article DOI: 10.1371/journal.pgen.1007248.].

FIN219/JAR1 and cryptochrome1 antagonize each other to modulate photomorphogenesis under blue light in Arabidopsis.

Plant development is affected by the integration of light and phytohormones, including jasmonates (JAs). To address the molecular mechanisms of possible interactions between blue light and JA signaling in Arabidopsis thaliana, we used molecular and transgenic approaches to understand the regulatory relationships between FAR-RED INSENSITIVE 219 (FIN219)/JASMONATE RESISTANT1 (JAR1) and the blue-light photoreceptor cryptochrome1 (CRY1). FIN219 overexpression in the wild type resulted in a short-hypocotyl phenotype under blue light. However, FIN219 overexpression in cry1, cry2 and cry1cry2 double mutant backgrounds resulted in phenotypes similar to their respective mutant backgrounds, which suggests that FIN219 function may require blue light photoreceptors. Intriguingly, FIN219 overexpression in transgenic plants harboring ectopic expression of the C terminus of CRY1 (GUS-CCT1), which exhibits a hypersensitive short-hypocotyl phenotype in all light conditions including darkness, led to a rescued phenotype under all light conditions except red light. Further expression studies showed mutual suppression between FIN219 and CRY1 under blue light. Strikingly, FIN219 overexpression in GUS-CCT1 transgenic lines (FIN219-OE/GUS-CCT1) abolished GUS-CCT1 fusion protein under blue light, whereas GUS-CCT1 fusion protein was stable in the fin219-2 mutant background (fin219-2/GUS-CCT1). Moreover, FIN219 strongly interacted with COP1 under blue light, and methyl JA (MeJA) treatment enhanced the interaction between FIN219 and GUS-CCT1 under blue light. Furthermore, FIN219 level affected GUS-CCT1 seedling responses such as anthocyanin accumulation and bacterial resistance under various light conditions and MeJA treatment. Thus, FIN219/JAR1 and CRY1 antagonize each other to modulate photomorphogenic development of seedlings and stress responses in Arabidopsis.