GmNAC039 and GmNAC018 activate the expression of cysteine protease genes to promote soybean nodule senescence.

Root nodules are major sources of nitrogen for soybean (Glycine max (L.) Merr.) growth, development, production, and seed quality. Symbiotic nitrogen fixation is time-limited, as the root nodule senesces during the reproductive stage of plant development, specifically during seed development. Nodule senescence is characterized by the induction of senescence-related genes, such as papain-like cysteine proteases (CYPs), which ultimately leads to the degradation of both bacteroids and plant cells. However, how nodule senescence-related genes are activated in soybean is unknown. Here, we identified 2 paralogous NAC transcription factors, GmNAC039 and GmNAC018, as master regulators of nodule senescence. Overexpression of either gene induced soybean nodule senescence with increased cell death as detected using a TUNEL assay, whereas their knockout delayed senescence and increased nitrogenase activity. Transcriptome analysis and nCUT&Tag-qPCR assays revealed that GmNAC039 directly binds to the core motif CAC(A)A and activates the expression of 4 GmCYP genes (GmCYP35, GmCYP37, GmCYP39, and GmCYP45). Similar to GmNAC039 and GmNAC018, overexpression or knockout of GmCYP genes in nodules resulted in precocious or delayed senescence, respectively. These data provide essential insights into the regulatory mechanisms of nodule senescence, in which GmNAC039 and GmNAC018 directly activate the expression of GmCYP genes to promote nodule senescence.

Ventral Tegmental Area Dysfunction and Disruption of Dopaminergic Homeostasis: Implications for Post-traumatic Stress Disorder.

Post-traumatic stress disorder (PTSD) is a debilitating psychiatric condition characterized by intrusive recollections of the traumatic event, avoidance behaviors, hyper-arousal to event-related cues, cognitive disruption, and mood dysregulation. Accumulating preclinical and clinical evidence implicates dysfunction of the ventral tegmental area (VTA) dopaminergic system in PTSD pathogenesis. This article reviews recent advances in our knowledge of the relationship between dopaminergic dyshomeostasis and PTSD, including the contributions of specific dopaminergic gene variants to disease susceptibility, alterations in VTA dopamine neuron activity, dysregulation of dopaminergic transmission, and potential pharmacological and psychological interventions for PTSD targeting the dopaminergic system. An in-depth understanding of PTSD etiology is crucial for the development of innovative risk assessment, diagnostic, and treatment strategies following traumatic events.