Metabolic signals influence cell-fate decisions in Dictyostelium discoideum.
AMPKα
Dictyostelium
ROS
Sir2D
differentiation
glucose
metabolites
Journal
Cell biochemistry and function
ISSN: 1099-0844
Titre abrégé: Cell Biochem Funct
Pays: England
ID NLM: 8305874
Informations de publication
Date de publication:
Dec 2023
Dec 2023
Historique:
revised:
15
11
2023
received:
18
08
2023
accepted:
16
11
2023
pubmed:
28
11
2023
medline:
28
11
2023
entrez:
28
11
2023
Statut:
ppublish
Résumé
Nutrient-sensing plays a crucial role in maintaining cellular energy and metabolic homeostasis. Perturbations in sensing pathways are associated with a wide variety of pathologies, especially metabolic diseases. Very little is understood about sensing fluctuations in nutrients and how this information is integrated into physiological and metabolic adaptation that could further affect cell-fate decisions during differentiation in Dictyostelium discoideum (henceafter, Dictyostelium). Glucose is the primary metabolic fuel among all nutrients. Carbohydrates, lipids and proteins ultimately breakdown into glucose, which is further used for providing energy. The maintenance of optimum glucose levels is important for efficient cell-survival. Glucose is not only a nutrient, but also a signaling molecule influencing cell growth and differentiation in Dictyostelium. Modulation of endogenous glucose levels either by varying exogenous glucose levels or genetic overexpression or deletion of genes involved in glucose signaling lead to changes in endogenous metabolite levels such as ADP/ATP ratio, NAD
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
1514-1525Subventions
Organisme : DBT BUILDER to SLS
ID : BT/INF/22/SP45382/2022
Organisme : Science and Engineering Research Board_NPDF
ID : Fellowship to Ibanylla Kynjai Hynniewta Hadem
Organisme : DST-FISTII to SLS
ID : SR/FST/LSII-046/2016C
Organisme : Department of Biotechnology, Ministry of Science and Technology, India
ID : Fellowship to Tasneem Fatima
Informations de copyright
© 2023 John Wiley & Sons Ltd.
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