The Amino Acid Transporter PtCAT7 and Ammonium Nutrition Enhance the Uptake of Thiamethoxam in Citrus Rootstock Seedlings.

Thiamethoxam (THX), when applied to the soil, can be taken up by citrus roots and subsequently transported to the leaves, providing effective protection of plants against the Asian citrus psyllid (Diaphorina citri Kuwayama). In this study, the field experiments showed that the coapplication of THX and nitrogen fertilizer (AN) did not affect THX uptake in six-year-old citrus plants. However, their coapplication promoted THX uptake in three-year-old Potassium trifoliate rootstocks and relieved the inhibition of AN at a higher level on plant growth characteristics, including biomass and growth of root and stem. RNA-seq analysis found that THX induced upregulation of a cationic amino acid transporter (PtCAT7) in citrus leaves. PtCAT7 facilitated THX uptake in the yeast strain to inhibit its growth, and the PtCAT7 protein was localized on the plasma membrane. Our results demonstrate that THX and N fertilizer can be coapplied and PtCAT7 may be involved in THX uptake in citrus.

The regulatory metabolic networks of the Brassica campestris L. hairy roots in response to cadmium stress revealed from proteome studies combined with a transcriptome analysis.

Brassica campestris L., a cadmium (Cd) hyperaccumulating herbaceous plant, is considered as a promising candidate for the bioremediation of Cd pollution. However, the molecular mechanisms regulating these processes remain unclear. The present work, using proteome studies combined with a transcriptome analysis, was carried out to reveal the response mechanisms of the hairy roots of Brassica campestris L. under Cd stress. Significant tissue necrosis and cellular damage occurred, and Cd accumulation was observed in the cell walls and vacuoles of the hairy roots. Through quantitative proteomic profiling, a total of 1424 differentially expressed proteins (DEPs) were identified, and are known to be enriched in processes including phenylalanine metabolism, plant hormone signal transduction, cysteine and methionine metabolism, protein export, isoquinoline alkaloid biosynthesis and flavone biosynthesis. Further studies combined with a transcriptome analysis found that 118 differentially expressed genes (DEGs) and their corresponding proteins were simultaneously up- or downregulated. Further Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analysis of the 118 shared DEGs and DEPs indicated their involvement in calcium, ROS and hormone signaling-mediated response, including regulation of carbohydrate and energy metabolism, biosynthesis of GSH, PCs and phenylpropanoid compounds that play vital roles in the Cd tolerance of Brassica campestris L. Our findings contribute to a better understanding of the regulatory networks of Brassica campestris L. under Cd stress, as well as provide valuable information on candidate genes (e.g., BrPAL, BrTAT, Br4CL, BrCDPK, BrRBOH, BrCALM, BrABCG1/2, BrVIP, BrGCLC, BrilvE, BrGST12/13/25). These results are of particular importance to the subsequent development of promising transgenic plants that will hyperaccumulate heavy metals and efficient phytoremediation processes.

Different drivers of soil C accumulation in aggregates in response to altered precipitation in a semiarid grassland.

Soil carbon (C) stabilization partially depends on its distribution within soil structural aggregates, and on the physicochemical processes of C within these aggregates. Changes in precipitation can alter the size distribution of aggregate classes within soils, and C input and output processes within these aggregates, which have potential consequences for soil C storage. However, the mechanisms underlying C accumulation within different aggregates under various precipitation regimes remain unclear. In this study, we conducted a 3-year field manipulation experiment to test the effects of a gradient of altered precipitation (-70%, -50%, -30%, 0%, +30%, and +50% amounts compared with ambient rainfall) on soil aggregate distribution and C accumulation in aggregates (53-250 µm, microaggregates; < 53 µm, silt and clay fractions) in a meadow steppe of northeastern China. Our results revealed that the distribution of soil microaggregates decreased along the precipitation gradient, with no detectable discrepant responses with respect to soil C accumulation within the microaggregates to precipitation treatments. In contrast, higher precipitation amounts coupled with a greater proportion of silt and clay fractions enhanced the accumulation of soil C. Importantly, structural equation models revealed that the pathways by which changes in precipitation control the accumulation of soil C varied across aggregate size fractions. Plant biomass was the main direct factor controlling the accumulation of C within soil microaggregates, whereas soil aggregate distribution and enzyme activities strongly interacted with soil C accumulation in the silt and clay fractions. Our findings imply that identifying how plant and soil aggregate properties respond to precipitation changes and drive C accumulation among soil particles will enhance the ability to predict responses of ecosystem processes to future global change.

Visual pigment-deficient cones survive and mediate visual signaling despite the lack of outer segments.

Rhodopsin and cone opsins are essential for light detection in vertebrate rods and cones, respectively. It is well established that rhodopsin is required for rod phototransduction, outer segment disk morphogenesis, and rod viability. However, the roles of cone opsins are less well understood. In this study, we adopted a loss-of-function approach to investigate the physiological roles of cone opsins in mice. We showed that cones lacking cone opsins do not form normal outer segments due to the lack of disk morphogenesis. Surprisingly, cone opsin-deficient cones survive for at least 12 mo, which is in stark contrast to the rapid rod degeneration observed in rhodopsin-deficient mice, suggesting that cone opsins are dispensable for cone viability. Although the mutant cones do not respond to light directly, they maintain a normal dark current and continue to mediate visual signaling by relaying the rod signal through rod-cone gap junctions. Our work reveals a striking difference between the role of rhodopsin and cone opsins in photoreceptor viability.

Tell Me More®: A medical student focused humanistic communication model to enhance student professional identity formation through meaningful patient encounters.

INTRODUCTION: The Tell Me More (TMM)® program provides a template for guided interviews to help providers procure an expansive social history from patients and connect with them as people beyond their illness. (TMM)® may provide a dual benefit: it improves the patient's experience with their healthcare team and the medical students' experience in developing their identity as a physician. Our aim was to characterize the impact of the patient-student conversations in TMM® on the participating medical students through analysis of their written reflections throughout the program. METHODS: Students conducted interviews with hospitalized patients using the TMM® template, Through narrative medicine and individualized posters, patients were able to highlight their unique qualities. RESULTS: Qualitative analyses of 63 journal reflections from 14 students, across 7 hospital settings, identified 6 themes. These included connection, humanism, discovery, impact, privilege, and perspective. CONCLUSION: Reflective practice as a learning pedagogy created an opportunity to enhance the medical students' awareness of empathy and compassion during the TMM® program. Documentation of reflections assured students would process the encounter as a profound learning experience and develop their professional identity formation as a student preparing to become a physician. PRACTICAL IMPLICATIONS: TMM® provides an opportunity for medical students to practice and apply their interpersonal and communication skills through authentic patient encounters.

Deletion of M-Opsin Prevents M Cone Degeneration in a Mouse Model of Leber Congenital Amaurosis.

Mutations in retinoid isomerase (RPE65) or lecithin-retinol acyltransferase (LRAT) disrupt 11-cis-retinal synthesis and cause Leber congenital amaurosis (LCA). Despite the success of recent RPE65 gene therapy, follow-up studies show that patients continue to experience photoreceptor degeneration and lose vision benefit over time. In Lrat-/- mouse model, mislocalized medium (M)-wavelength opsin was degraded, whereas mislocalized short (S)-wavelength opsin accumulated before the onset of cone degeneration. The mechanism for the foveal M/long-wavelength cone photoreceptor degeneration in LCA is unknown. By crossing Lrat-/- mice with a proteasome reporter mouse strain, this study showed that M-opsin-enriched dorsal cones in Lrat-/- mice exhibit proteasome stress because of the degradation of large amounts of M-opsin. Deletion of M-opsin relieves the proteasome stress and completely prevents M cone degeneration in Lrat-/-Opn1sw-/- mice (a pure M cone LCA model, Opn1sw encoding S-opsin) for at least 12 months. These results suggest that M-opsin degradation-associated proteasome stress plays a major role in M cone degeneration in Lrat-/- model. This finding may represent a general mechanism for M cone degeneration in multiple forms of cone degeneration because of M-opsin mislocalization and degradation. These results have important implications for the current gene therapy strategy for LCA that emphasizes the need for combinatorial therapies to both improve vision and slow photoreceptor degeneration.