Biology subjects

Asim, M.

Publications and source records attributed to Asim, M..

3 recordsLinked to original sources

bioRxiv2025

Hyperactivity of the Amygdala Mediates Depressive-Like Phenotypes and Decreased Serotonin Release

Clinical and preclinical studies have consistently demonstrated a correlation between hyperactivity of the amygdala and the onset of depression. However, the underlying mechanisms influencing serotonin levels a critical neurotransmitter implicated in depression and a primary target for selective serotonin reuptake inhibitors (SSRIs) remain inadequately understood. In this study, we employed a restrained inescapable shock (RIS) model to investigate these mechanisms in mice. The RIS paradigm elicited depressive-like phenotypes, increased c-Fos expression in the amygdala, diminished serotonin levels, and elevated corticosterone concentrations. Notably, chemogenetic inhibition of the amygdala mitigated depressive symptoms, reduced neuronal activity in this region, and restored serotonin levels. Anatomical analyses revealed a significant connectivity between the central amygdala (CeA) and the dorsal raphe nucleus (DRN). Fiber photometry recordings indicated that serotonergic neuronal activity in the DRN decreased in response to aversive stimuli, accompanied by amygdala activation following RIS, with no notable alterations in DRN GABAergic activity. These findings suggest that chronic stress may exacerbate amygdala hyperactivity, which subsequently inhibits serotonin release in the brain, potentially intensifying depressive states. Therefore, targeting amygdala hyperactivity may represent a novel therapeutic strategy for the management of stress-related depressive and anxiety disorders.

neuroscience↗

bioRxiv2022

Strigolactone mediates moso bamboo root response to phosphate stress

Moso bamboo (Phyllostachys edulis) grows in soils with widespread phosphate (Pi) deficiency, resulting in low shoot yield. While it also suffers from high Pi due to heavy fertilization, which causes the degradation of bamboo forest. A novel plant hormone, strigolactone (SL), plays a key role in root growth and development under Pi stress, but its regulatory mechanism has not been systematically reported. Our study investigated SL-mediated mechanism in response to Pi stress in moso bamboo. We compared the root growth under low, sufficient and high Pi, and analyzed the temporary trends of gene expression in primary root tip region and lateral root primordium zone. The effects of SL-analog (GR24) and SL-inhibitor (TIS108) on root architecture at low and high Pi were evaluated. SL biosynthesis and signaling are the main pathways of root response to Pi stress. With the decrease of Pi level, 5-deoxystrigol and strigol in the root exudates increase significantly. Under low Pi, SL is indispensable for the maintenance of root cell morphology, and promotes primary root elongation and reduces lateral root formation by upregulating the expression of phosphorous starvation response genes and downregulating the expression of abscisic acid response genes. The absence of SL at high Pi releases the inhibition of ethylene responsive genes expression to inhibit root elongation and promote branching. In general, SL mediates the response of bamboo roots to Pi stress by regulating its biosynthesis and signal transduction and influencing other hormone pathways.

molecular biology↗

bioRxiv2020

Transcriptional network involving ERG and AR orchestrates Distal-Less Homeobox 1 mediated prostate cancer progression.

Nearly half of the prostate cancer (PCa) cases show elevated levels of ERG oncoprotein due to TMPRSS2-ERG gene fusion. Here, we demonstrate ERG mediated upregulation of Distal-less homeobox-1 (DLX1), an established PCa biomarker. Using series of functional assays, we show DLX1 elicits oncogenic properties in prostate epithelial cells, and abrogating its function leads to reduced tumor burden in mouse xenografts. Clinically, [~]60% of the PCa patients exhibit high DLX1 levels, while [~]50% of these cases also harbor elevated ERG associated with aggressive disease and poor survival probability. Mechanistically, we show that ERG gets recruited onto DLX1 promoter and interacts with its enhancer-bound androgen receptor (AR) and FOXA1 to regulate DLX1 expression in TMPRSS2-ERG positive cases. Alternatively, in ERG-negative cases, DLX1 is regulated by AR/AR-V7 and FOXA1. Importantly, BET bromodomain inhibitors disrupt the transcriptional regulators of DLX1 and its associated oncogenic properties, signifying their efficacy in treatment of DLX1-positive PCa patients.

cancer biology↗