Jasmonate activates secondary cell wall biosynthesis through MYC2-MYB46 module.

Formation of secondary cell wall (SCW) is tightly regulated spatiotemporally by various developmental and environmental signals. Successful fine-tuning of the trade-off between SCW biosynthesis and stress responses requires a better understanding of how plant growth is regulated under environmental stress conditions. However, the current understanding of the interplay between environmental signaling and SCW formation is limited. The lipid-derived plant hormone jasmonate (JA) and its derivatives are important signaling components involved in various physiological processes including plant growth, development, and abiotic/biotic stress responses. Recent studies suggest that JA is involved in SCW formation but the signaling pathway has not been studied for how JA regulates SCW formation. We tested this hypothesis using the transcription factor MYB46, a master switch for SCW biosynthesis, and JA treatments. Both the transcript and protein levels of MYB46, a master switch for SCW formation, were significantly increased by JA treatment, resulting in the upregulation of SCW biosynthesis. We then show that this JA-induced upregulation of MYB46 is mediated by MYC2, a central regulator of JA signaling, which binds to the promoter of MYB46. We conclude that this MYC2-MYB46 module is a key component of the plant response to JA in SCW formation.

The biology of time: dynamic responses of cell types to developmental, circadian and environmental cues.

As sessile organisms, plants are finely tuned to respond dynamically to developmental, circadian and environmental cues. Genome-wide studies investigating these types of cues have uncovered the intrinsically different ways they can impact gene expression over time. Recent advances in single-cell sequencing and time-based bioinformatic algorithms are now beginning to reveal the dynamics of these time-based responses within individual cells and plant tissues. Here, we review what these techniques have revealed about the spatiotemporal nature of gene regulation, paying particular attention to the three distinct ways in which plant tissues are time sensitive. (i) First, we discuss how studying plant cell identity can reveal developmental trajectories hidden in pseudotime. (ii) Next, we present evidence that indicates that plant cell types keep their own local time through tissue-specific regulation of the circadian clock. (iii) Finally, we review what determines the speed of environmental signaling responses, and how they can be contingent on developmental and circadian time. By these means, this review sheds light on how these different scales of time-based responses can act with tissue and cell-type specificity to elicit changes in whole plant systems.

Nucleocytoplasmic partitioning as a mechanism to regulate Arabidopsis signaling events.

The nucleus is the site of transcription events - compartmentalization of transcription in eukaryotes allows for regulated access to chromatin. The nucleopore, a complex of many intrinsically disorder proteins, acts as the gatekeeper for nuclear entry and exit, and receptors for nuclear localization signals and nuclear export signals interact with both cargo and nucleopore components to facilitate this movement. Thus, regulated occlusion of the nuclear localization signal or nuclear export signal, tethering of proteins, or sequestration in biomolecular condensates can be used to regulate nucleocytoplasmic partitioning. In plants, regulated nucleocytoplasmic partitioning is a key mechanism to regulate signaling pathways, including those involved in various phytohormones, environmental stimuli, and pathogen responses.

Environmental mechanisms of orofacial clefts.

Orofacial clefts (OFCs) are among the most common birth defects and impart a significant burden on afflicted individuals and their families. It is increasingly understood that many nonsyndromic OFCs are a consequence of extrinsic factors, genetic susceptibilities, and interactions of the two. Therefore, understanding the environmental mechanisms of OFCs is important in the prevention of future cases. This review examines the molecular mechanisms associated with environmental factors that either protect against or increase the risk of OFCs. We focus on essential metabolic pathways, environmental signaling mechanisms, detoxification pathways, behavioral risk factors, and biological hazards that may disrupt orofacial development.

Circadian Regulation of the Plant Transcriptome Under Natural Conditions.

Circadian rhythms produce a biological measure of the time of day. In plants, circadian regulation forms an essential adaptation to the fluctuating environment. Most of our knowledge of the molecular aspects of circadian regulation in plants is derived from laboratory experiments that are performed under controlled conditions. However, it is emerging that the circadian clock has complex roles in the coordination of the transcriptome under natural conditions, in both naturally occurring populations of plants and in crop species. In this review, we consider recent insights into circadian regulation under natural conditions. We examine how circadian regulation is integrated with the acute responses of plants to the daily and seasonally fluctuating environment that also presents environmental stresses, in order to coordinate the transcriptome and dynamically adapt plants to their continuously changing environment.

Direct Control of SPEECHLESS by PIF4 in the High-Temperature Response of Stomatal Development.

Environmental factors shape the phenotypes of multicellular organisms. The production of stomata-the epidermal pores required for gas exchange in plants-is highly plastic and provides a powerful platform to address environmental influence on cell differentiation [1-3]. Rising temperatures are already impacting plant growth, a trend expected to worsen in the near future [4]. High temperature inhibits stomatal production, but the underlying mechanism is not known [5]. Here, we show that elevated temperature suppresses the expression of SPEECHLESS (SPCH), the basic-helix-loop-helix (bHLH) transcription factor that serves as the master regulator of stomatal lineage initiation [6, 7]. Our genetic and expression analyses indicate that the suppression of SPCH and stomatal production is mediated by the bHLH transcription factor PHYTOCHROME-INTERACTING FACTOR 4 (PIF4), a core component of high-temperature signaling [8]. Importantly, we demonstrate that, upon exposure to high temperature, PIF4 accumulates in the stomatal precursors and binds to the promoter of SPCH. In addition, we find SPCH feeds back negatively to the PIF4 gene. We propose a model where warm-temperature-activated PIF4 binds and represses SPCH expression to restrict stomatal production at elevated temperatures. Our work identifies a molecular link connecting high-temperature signaling and stomatal development and reveals a direct mechanism by which production of a specific cell lineage can be controlled by a broadly expressed environmental signaling factor.

Soil Lead and Children's Blood Lead Disparities in Pre- and Post-Hurricane Katrina New Orleans (USA).

This study appraises New Orleans soil lead and children's lead exposure before and ten years after Hurricane Katrina flooded the city. Introduction: Early childhood exposure to lead is associated with lifelong and multiple health, learning, and behavioral disorders. Lead exposure is an important factor hindering the long-term resilience and sustainability of communities. Lead exposure disproportionately affects low socioeconomic status of communities. No safe lead exposure is known and the common intervention is not effective. An essential responsibility of health practitioners is to develop an effective primary intervention. Methods: Pre- and post-Hurricane soil lead and children's blood lead data were matched by census tract communities. Soil lead and blood lead data were described, mapped, blood lead graphed as a function of soil lead, and Multi-Response Permutation Procedures statistics established disparities. Results: Simultaneous decreases occurred in soil lead accompanied by an especially large decline in children's blood lead 10 years after Hurricane Katrina. Exposure disparities still exist between children living in the interior and outer areas of the city. Conclusions: At the scale of a city, this study demonstrates that decreasing soil lead effectively reduces children's blood lead. Primary prevention of lead exposure can be accomplished by reducing soil lead in the urban environment.

Genome-Wide Transcriptional Profiling to Elucidate Key Candidates Involved in Bud Burst and Rattling Growth in a Subtropical Bamboo (Dendrocalamus hamiltonii).

Bamboo, one of the fastest growing plants, can be a promising model system to understand growth. The study provides an insight into the complex interplay between environmental signaling and cellular machineries governing initiation and persistence of growth in a subtropical bamboo (Dendrocalamus hamiltonii). Phenological and spatio-temporal transcriptome analysis of rhizome and shoot during the major vegetative developmental transitions of D. hamiltonii was performed to dissect factors governing growth. Our work signifies the role of environmental cues, predominantly rainfall, decreasing day length, and high humidity for activating dormant bud to produce new shoot, possibly through complex molecular interactions among phosphatidylinositol, calcium signaling pathways, phytohormones, circadian rhythm, and humidity responses. We found the coordinated regulation of auxin, cytokinin, brassinosteroid signaling and cell cycle modulators; facilitating cell proliferation, cell expansion, and cell wall biogenesis supporting persistent growth of emerging shoot. Putative master regulators among these candidates were identified using predetermined Arabidopsis thaliana protein-protein interaction network. We got clues that the growth signaling begins far back in rhizome even before it emerges out as new shoot. Putative growth candidates identified in our study can serve in devising strategies to engineer bamboos and timber trees with enhanced growth and biomass potentials.

Environmental signaling: from environmental estrogens to endocrine-disrupting chemicals and beyond.

The landmark report (Herbst et al. 1971) linking prenatal treatment with a synthetic estrogen, diethylstilbestrol (DES), to cancer at puberty in women whose mothers took the drug while pregnant ushered in an era of research on delayed effects of such exposures on functional outcomes in offspring. An animal model developed in our laboratory at the National Institute of Environmental Health Sciences confirmed that DES was the carcinogen and exposure to DES caused, as well, functional alterations in the reproductive, endocrine, and immune systems of male and female mice treated in utero. DES was also being used in agriculture and we discovered, at the first meeting on Estrogens in the Environment in 1979 (Estrogens in the Environment, 1980), that many environmental contaminants were also estrogenic. Many laboratories sought to discern the basis for estrogenicity in environmental chemicals and to discover other hormonally active xenobiotics. Our laboratory elucidated how DES and other estrogenic compounds worked by altering differentiation through epigenetic gene imprinting, helping explain the transgenerational effects found in mice and humans. At the Wingspread Conference on the Human-Wildlife Connection in 1991 (Advances in Modern Environmental Toxicology, 1992), we learned that environmental disruption of the endocrine system occurred in many species and phyla, and the term endocrine disruption was introduced. Further findings of transgenerational effects of environmental agents that mimicked or blocked various reproductive hormones and the ubiquity of environmental signals, such as bisphenol A increased concern for human and ecological health. Scientists began to look at other endocrine system aspects, such as cardiovascular and immune function, and other nuclear receptors, with important observations regarding obesity and metabolism. Laboratories, such as ours, are now using stem cells to try to understand the mechanisms by which various environmental signals alter cell differentiation. Since 2010, research has shown that trauma and other behavioral inputs can function as 'environmental signals,' can be encoded in gene regulation networks in a variety of cells and organs, and can be passed on to subsequent generations. So now we come full circle: environmental chemicals mimic hormones or other metabolic signaling molecules and now behavioral experience can be transduced into chemical signals that also modify gene expression.