NAD(P) transhydrogenase isoform distribution provides insight into apicomplexan evolution.

Front Ecol Evol

Department of Infection Biology, Faculty of Infectious and Tropical Diseases, London School of Hygiene & Tropical Medicine, Keppel Street, London WC1E 7HT, United Kingdom.

Published: June 2023


Category Ranking

98%

Total Visits

921

Avg Visit Duration

2 minutes

Citations

20

Article Abstract

Membrane-located NAD(P) transhydrogenase (NTH) catalyses reversible hydride ion transfer between NAD(H) and NADP(H), simultaneously translocating a proton across the membrane. The enzyme is structurally conserved across prokaryotes and eukaryotes. In heterotrophic bacteria NTH proteins reside in the cytoplasmic membrane, whereas in animals they localise in the mitochondrial inner membrane. Eukaryotic NTH proteins exists in two distinct configurations (isoforms) and have non-mitochondrial functions in unicellular eukaryotes like , the causative agent of malaria. In this study, we carried out a systematic analysis of genes across eukaryotic life to determine its prevalence and distribution of isoforms. The results reveal that NTH is found across all major lineages, but that some organisms, notably plants, lack genes altogether. Isoform distribution and phylogenetic analysis reveals different gene loss scenarios in apicomplexan lineages, which sheds new light on the evolution of the Piroplasmida and .

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7614955PMC
http://dx.doi.org/10.3389/fevo.2023.1216385DOI Listing

Publication Analysis

Top Keywords

nadp transhydrogenase
8
isoform distribution
8
nth proteins
8
transhydrogenase isoform
4
distribution insight
4
insight apicomplexan
4
apicomplexan evolution
4
evolution membrane-located
4
membrane-located nadp
4
nth
4

Similar Publications

Backgrounds: Premature diffuse familial sebaceous hyperplasia (PDFSH) constitutes a distinct clinical variant of sebaceous hyperplasia, characterized by three hallmark features: early disease onset, characteristic sparing of perioral and periocular regions, and a positive family history. To date, the pathogenic gene underlying PDFSH remains unidentified.

Objectives: The aim of this study was to identify the underlying gene and the pathogenesis of three familial cases with autosomal dominant PDFSH.

View Article and Find Full Text PDF

Carboxylate chain elongation can create value-added bioproducts from waste activated sludge (WAS). The bioconversion of WAS during anaerobic fermentation is often constrained by inefficient hydrolysis. The addition of MOF-808 (200 mg MOF-808/g volatile solids (VS)) increased caproate production and selectivity by approximately 38.

View Article and Find Full Text PDF

Mitochondrial NNT Promotes Diastolic Dysfunction in Cardiometabolic HFpEF.

Circ Res

June 2025

Medical Faculty Heidelberg, Institute of Experimental Cardiology (M.E.P., P.J.M.K., S.N., F.B., F.S., M.D., J.B.), Heidelberg University, Germany.

Background: Clinical management of heart failure with preserved ejection fraction (HFpEF) is hindered by a lack of disease-modifying therapies capable of altering its distinct pathophysiology. Despite the widespread implementation of a 2-hit model of cardiometabolic HFpEF to inform precision therapy, which utilizes HFD+L-NAME (ad libitum high-fat diet and 0.5% N[ω]-nitro-L-arginine methyl ester), we observe that C57BL6/J mice exhibit less cardiac diastolic dysfunction in response to HFD+L-NAME.

View Article and Find Full Text PDF

Scutellarein (Sc), a natural flavonoid, holds potential for treating pulmonary arterial hypertension (PAH), yet its mechanisms remain unexplored. This study investigated Sc's therapeutic effects and underlying pathways in PAH. In vivo experiments demonstrated that Sc significantly attenuated right ventricular hypertension, pulmonary arterial remodeling, αSMA expression, and vascular inflammation in PAH models.

View Article and Find Full Text PDF

The human mitochondrial nicotinamide nucleotide transhydrogenase (NNT) uses the proton motive force to drive hydride transfer from NADH to NADP and is a major contributor to the generation of mitochondrial NADPH. NNT plays a critical role in maintaining cellular redox balance. NNT-deficiency results in oxidative damage and its absence results in familial glucocorticoid deficiency.

View Article and Find Full Text PDF