Background: Plastic is everywhere. It is used in food packaging, storage containers, electronics, furniture, clothing, and common single-use disposable items. Microplastic and nanoplastic particulates are formed from bulk fragmentation and disintegration of plastic pollution. Plastic particulates have recently been detected in indoor air and remote atmospheric fallout. Due to their small size, microplastic and nanoplastic particulate in the atmosphere can be inhaled and may pose a risk for human health, speci cally in susceptible populations. When inhaled, nanosized particles have been shown to translocate across pulmonary cell barriers to secondary organs, including the placenta. However, the potential for maternal-to-fetal translocation of nanosized-plastic particles and the impact of nanoplastic deposition and accumulation on fetal health remain unknown. In this study we investigated whether nanopolystyrene particles can cross the placental barrier and deposit in fetal tissues after maternal pulmonary exposure. Results: Pregnant Sprague Dawley rats were exposed to 20 nm rhodamine-labeled nanopolystyrene beads (2.64 x 10 14 particles) via intratracheal instillation on gestational day (GD) 19. Twenty-four hours later on GD 20, maternal and fetal tissues were evaluated using uorescent optical imaging. Fetal tissues were xed for particle visualization with hyperspectral microscopy. Using isolated placental perfusion, a known concentration of nanopolystyrene was injected into the uterine artery. Maternal and fetal e uents were collected for 180 minutes and assessed for polystyrene particle concentration. Twenty-four hours after maternal exposure, fetal and placental weights were signi cantly lower (7% and 8%, respectively) compared with controls. Nanopolystyrene particles were detected in the maternal lung, heart, and spleen. Polystyrene nanoparticles were also observed in the placenta, fetal liver, lungs, heart, kidney, and brain suggesting maternal lung-to-fetal tissue nanoparticle translocation in late stage pregnancy. Conclusion: These studies con rm that maternal pulmonary exposure to nanopolystyrene results in the translocation of plastic particles to placental and fetal tissues and renders the fetoplacental unit vulnerable to adverse effects. These data are vital to the understanding of plastic particulate toxicology and the developmental origins of health and disease. Background Plastics are ubiquitous in modern society, used worldwide in a variety of applications ranging from manufacturing, packaging materials, personal products, and medical devices. Growing production and post-consumer plastic waste disposal contribute to the accumulation of plastic in land lls, waterways, and oceans [1]. In the natural environment, material fragmentation of bulk plastic waste by a combination of physical, chemical, and biological processes produces smaller particles referred to as microplastics (< 5 mm in a single dimension [2]) and nanoplastics (< 100 nm in a single dimension). Recent literature identi ed microplastics ...

MYB transcription factors (TFs) play pivotal roles in the abiotic stress response in plants, but their characteristics and functions in wheat (Triticum aestivum L.) have not been fully investigated. A novel wheat MYB TF gene, TaMYB73, is reported here based on the observation that its targeting probe showed the highest salinity-inducibility level among all probes annotated as MYB TFs in the cDNA microarray. TaMYB73 is a R2R3 type MYB protein with transactivation activity, and binds with types I, II, and IIG MYB binding motifs. The gene was induced by NaCl, dehydration, and several phytohormones, as well as some stress-, ABA-, and GA-responsive cis-elements present in its promoter region. Its over-expression in Arabidopsis enhanced the tolerance to NaCl as well as to LiCl and KCl, whereas it had no contribution to mannitol tolerance. The over-expression lines had superior germination ability under NaCl and ABA treatments. The expression of many stress signalling genes such as AtCBF3 and AtABF3, as well as downstream responsive genes such as AtRD29A and AtRD29B, was improved in these over-expression lines, and TaMYB73 can bind with promoter sequences of AtCBF3 and AtABF3. Taken together, it is suggested that TaMYB73, a novel MYB transcription factor gene, participates in salinity tolerance based on improved ionic resistance partly via the regulation of stress-responsive genes.

The core regulators which are required for primary root growth and development also function in lateral root development or lateral root stem cell niche maintenance. The primary root systems and the lateral root systems are the two important root systems which are vital to the survival of plants. Though the molecular mechanism of the growth and development of both the primary root systems and the lateral root systems have been extensively studied individually in Arabidopsis, there are not so much evidence to show that if both root systems share common regulatory mechanisms. AP2 family transcription factors such as PLT1 (PLETHORA1) and PLT2, GRAS family transcription factors such as SCR (SCARECROW) and SHR (SHORT ROOT) and WUSCHEL-RELATED HOMEOBOX transcription factor WOX5 have been extensively studied and found to be essential for primary root growth and development. In this study, through the expression pattern analysis and mutant examinations, we found that these core regulators also function in lateral root development or lateral root stem cell niche maintenance.

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Shade avoidance syndrome (SAS) arises in densely growing plants that compete for light. In Arabidopsis thaliana, phytochrome interacting factor (PIF) proteins link the perception of shade to stem elongation via auxin production. Here, we report that PIFs inhibit the shade-induced expression of AUXIN RESPONSE FACTOR 18 (ARF18), and ARF18 represses auxin signaling. Therefore, PIF-mediated inhibition of ARF18 enhances auxin-dependent hypocotyl elongation in simulated shade. Furthermore, we show that both PIFs and ARF18 directly repress qua-quine starch (QQS), which controls the allocation of carbon and nitrogen. Shade-repressed QQS attenuates the conversion of starch to protein and thus reduced leaf area. Our results suggest that PIF-dependent gene regulation coordinates multiple SAS responses, including altered stem growth via ARF18, as well as altered leaf growth and metabolism via QQS.