PISD

Last update 08 May 2025

Basic Info

Synonyms

dJ858B16.2, phosphatidylserine decarboxylase, Phosphatidylserine decarboxylase alpha chain

+ [4]

Introduction

Catalyzes the formation of phosphatidylethanolamine (PtdEtn) from phosphatidylserine (PtdSer) (PubMed:30488656, PubMed:30858161). Plays a central role in phospholipid metabolism and in the interorganelle trafficking of phosphatidylserine. May be involved in lipid droplet biogenesis at the endoplasmic reticulum membrane (By similarity).

100 Clinical Results associated with PISD

100 Translational Medicine associated with PISD

0 Patents (Medical) associated with PISD

209

Literatures (Medical) associated with PISD

02 Jan 2025·Autophagy

Mitochondrial bioenergetics stimulates autophagy for pathological MAPT/Tau clearance in tauopathy neurons

Article

Author: Nissenbaum, Marialaina ; Rajapaksha, Gavesh ; Jia, Nuo ; Guan, Hongyuan ; Kusnecov, Alexander W. ; Cai, Qian ; Jeong, Yu Young ; Ganesan, Dhasarathan ; Han, Sinsuk

Hyperphosphorylation and aggregation of MAPT (microtubule-associated protein tau) is a pathogenic hallmark of tauopathies and a defining feature of Alzheimer disease (AD). Pathological MAPT/tau is targeted by macroautophagy/autophagy for clearance after being sequestered within autophagosomes, but autophagy dysfunction is indicated in tauopathy. While mitochondrial bioenergetic deficits have been shown to precede MAPT/tau pathology in tauopathy brains, it is unclear whether energy metabolism deficiency is involved in the pathogenesis of autophagy defects. Here, we reveal that stimulation of anaplerotic metabolism restores defective oxidative phosphorylation (OXPHOS) in tauopathy neurons which, strikingly, leads to pronounced MAPT/tau clearance by boosting autophagy functionality through enhancements of mitochondrial biosynthesis and supply of phosphatidylethanolamine for autophagosome biogenesis. Furthermore, early anaplerotic stimulation of OXPHOS elevates autophagy activity and attenuates MAPT/tau pathology, thereby counteracting memory impairment in tauopathy mice. Taken together, our study sheds light on a pivotal role of mitochondrial bioenergetic deficiency in tauopathy-related autophagy defects and suggests a new therapeutic strategy to prevent the buildup of pathological MAPT/tau in AD and other tauopathy diseases.Abbreviation: AA: antimycin A; AD, Alzheimer disease; ATP, adenosine triphosphate; AV, autophagosome/autophagic vacuole; AZ, active zone; Baf-A1: bafilomycin A₁; CHX, cycloheximide; COX, cytochrome c oxidase; DIV, days in vitro; DRG, dorsal root ganglion; ETN, ethanolamine; FRET, Förster/fluorescence resonance energy transfer; FTD, frontotemporal dementia; Gln, glutamine; HA: hydroxylamine; HsMAPT/Tau, human MAPT; IMM, inner mitochondrial membrane; LAMP1, lysosomal-associated membrane protein 1; LIs, lysosomal inhibitors; MDAV, mitochondria-derived autophagic vacuole; MmMAPT/Tau, murine MAPT; NFT, neurofibrillary tangle; OCR, oxygen consumption rate; Omy: oligomycin; OXPHOS, oxidative phosphorylation; PPARGC1A/PGC-1alpha: peroxisome proliferative activated receptor, gamma, coactivator 1 alpha; PE, phosphatidylethanolamine; phospho-MAPT/tau, hyperphosphorylated MAPT; PS, phosphatidylserine; PISD, phosphatidylserine decarboxylase;SQSTM1/p62, sequestosome 1; STX1, syntaxin 1; SYP, synaptophysin; Tg, transgenic; TCA, tricarboxylic acid; TEM, transmission electron microscopy.

01 Dec 2024·Applied Microbiology and Biotechnology

Membrane protein Bcsdr2 mediates biofilm integrity, hyphal growth and virulence of Botrytis cinerea

Article

Author: Ge, Beibei ; Shi, Liming ; Li, Hua ; Zhang, Wei ; Zhang, Kecheng ; Cao, Yi ; Rasmey, Abdel-Hamied M

AbstractGrey mould caused by Botrytis cinerea is a devastating disease responsible for large losses to agricultural production, and B. cinerea is a necrotrophic model fungal plant pathogen. Membrane proteins are important targets of fungicides and hotspots in the research and development of fungicide products. Wuyiencin affects the permeability and pathogenicity of B. cinerea, parallel reaction monitoring revealed the association of membrane protein Bcsdr2, and the bacteriostatic mechanism of wuyiencin was elucidated. In the present work, we generated and characterised ΔBcsdr2 deletion and complemented mutant B. cinerea strains. The ΔBcsdr2 deletion mutants exhibited biofilm loss and dissolution, and their functional activity was illustrated by reduced necrotic colonisation on strawberry and grape fruits. Targeted deletion of Bcsdr2 also blocked several phenotypic defects in aspects of mycelial growth, conidiation and virulence. All phenotypic defects were restored by targeted gene complementation. The roles of Bcsdr2 in biofilms and pathogenicity were also supported by quantitative real-time RT-PCR results showing that phosphatidylserine decarboxylase synthesis gene Bcpsd and chitin synthase gene BcCHSVII were downregulated in the early stages of infection for the ΔBcsdr2 strain. The results suggest that Bcsdr2 plays important roles in regulating various cellular processes in B. cinerea.Key points• The mechanism of wuyiencin inhibits B. cinerea is closely associated with membrane proteins.• Wuyiencin can downregulate the expression of the membrane protein Bcsdr2 in B. cinerea.• Bcsdr2 is involved in regulating B. cinerea virulence, growth and development.

01 Dec 2024·Alzheimer's & Dementia

Multi‐omics assessment of genotype and sex‐specific effects of organochlorine pesticide DDT in humanized APOE mice

Article

Author: Richardson, Jason R ; Eid, Aseel ; Zhan, Jiada J ; Hart, Ronald P ; Go, Young‐Mi ; Han, Yoonhee ; Mhatre‐Winters, Isha ; Barahona, Arturo J ; Jones, Dean P ; Tran, ViLinh

AbstractBackgroundThe Apolipoprotein‐E (APOE) ε4 gene variant is the strongest genetic risk factor for late‐onset Alzheimer’s Disease, but is not entirely predictive. Emerging evidence suggests environmental factors contribute to disease etiology, with epidemiological studies associating pesticide exposure with lower cognitive scores. Dichlorodiphenyltrichloroethane (DDT), a pesticide used extensively in the US until 1972, persists in trace amounts due to its long half‐life, bioaccumulation, and existing dumpsites. We have previously reported that DDT induces AD pathology in multiple models and also shown increased serum levels of DDE, the primary metabolite of DDT, in AD patients, where APOE genotype modified MMSE scores and contributed a ∼4‐fold increase in AD risk. Here, we sought to identify the mechanism(s) by which APOE4 genotype alters pathological response to DDT by a multi‐omics approach.MethodTo assess the effects of DDT exposure, three‐month‐old male and female APOE3 (E3) and APOE4 (E4) mice were exposed to 3 mg/kg DDT by oral gavage every 3 days for 5 months. Hippocampus was dissected out and frozen for RNA‐sequencing and metabolomic analysis, while serum was collected for metabolomic analysis and biomarker measurement.ResultRNA‐sequencing analysis between genotypes of female DDT‐exposed mice indicated significantly downregulated pathways and functions (p<0.05) in the hippocampus of E4‐females, including phosphatidylserine decarboxylase activity and neuron projection. Similarly, DDT‐exposed E4‐males indicated downregulation of ion channel regulator activity, nucleotide binding, cell‐cell and synaptic signaling, and neuron projection. Further, untargeted metabolomic analysis of DDT‐exposed mice was compared. Top pathways (p<0.05) altered in E4 vs. E3 female‐DDT hippocampus were carnitine shuttle and glycolysis‐gluconeogenesis, while serum changes included TCA cycle and tryptophan metabolism. In E4 vs. E3 male‐DDT, hippocampal alterations included purine metabolism, fatty acid mitochondrial beta‐oxidation, TCA cycle, glycolysis, and carnitine shuttle, while serum changes involved cholesterol biosynthesis, TCA cycle, and glycolysis‐gluconeogenesis. Finally, DDT increased serum neurofilament light chain (NfL) levels, a biomarker for neurodegeneration, by 1.9 and 2.1‐fold in E4‐male and E4‐female mice compared to respective controls. NfL was 1.4‐fold higher in DDT‐exposed E4‐females compared to E4‐males.ConclusionThese data demonstrate gene‐by‐environment interactions modified by sex, providing a platform to investigate mechanisms in AD‐related neurodegeneration and corroborating previous epidemiological findings.

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