About: Glucose 6-phosphate dehydrogenase deficiency enhances germ cell apoptosis and causes defective embryogenesis in Caenorhabditis elegans

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About: Glucose 6-phosphate dehydrogenase deficiency enhances germ cell apoptosis and causes defective embryogenesis in Caenorhabditis elegans Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Glucose 6-phosphate dehydrogenase deficiency enhances germ cell apoptosis and causes defective embryogenesis in Caenorhabditis elegans
Creator	Chen, T-L Cheng, K-P Cheng, M-L Ho, H-Y Lin, Y-H Wu, Y-H Yang, H-C Chiu, Dt-Y Lo, S
topic	covid:e0187a691be1237e922515d56bcfbc7ec988fa3e#this
Source	Medline; PMC
abstract	Glucose 6-phosphate dehydrogenase (G6PD) deficiency, known as favism, is classically manifested by hemolytic anemia in human. More recently, it has been shown that mild G6PD deficiency moderately affects cardiac function, whereas severe G6PD deficiency leads to embryonic lethality in mice. How G6PD deficiency affects organisms has not been fully elucidated due to the lack of a suitable animal model. In this study, G6PD-deficient Caenorhabditis elegans was established by RNA interference (RNAi) knockdown to delineate the role of G6PD in animal physiology. Upon G6PD RNAi knockdown, G6PD activity was significantly hampered in C. elegans in parallel with increased oxidative stress and DNA oxidative damage. Phenotypically, G6PD-knockdown enhanced germ cell apoptosis (2-fold increase), reduced egg production (65% of mock), and hatching (10% of mock). To determine whether oxidative stress is associated with G6PD knockdown-induced reproduction defects, C. elegans was challenged with a short-term hydrogen peroxide (H(2)O(2)). The early phase egg production of both mock and G6PD-knockdown C. elegans were significantly affected by H(2)O(2). However, H(2)O(2)-induced germ cell apoptosis was more dramatic in mock than that in G6PD-deficient C. elegans. To investigate the signaling pathways involved in defective oogenesis and embryogenesis caused by G6PD knockdown, mutants of p53 and mitogen-activated protein kinase (MAPK) pathways were examined. Despite the upregulation of CEP-1 (p53), cep-1 mutation did not affect egg production and hatching in G6PD-deficient C. elegans. Neither pmk-1 nor mek-1 mutation significantly affected egg production, whereas sek-1 mutation further decreased egg production in G6PD-deficient C. elegans. Intriguingly, loss of function of sek-1 or mek-1 dramatically rescued defective hatching (8.3- and 9.6-fold increase, respectively) induced by G6PD knockdown. Taken together, these findings show that G6PD knockdown reduces egg production and hatching in C. elegans, which are possibly associated with enhanced oxidative stress and altered MAPK pathways, respectively.
has issue date	2013-05-02(xsd:dateTime)
bibo:doi	10.1038/cddis.2013.132
bibo:pmid	23640458
has license	cc-by-nc-nd
sha1sum (hex)	e0187a691be1237e922515d56bcfbc7ec988fa3e
schema:url	https://doi.org/10.1038/cddis.2013.132
resource representing a document's title	Glucose 6-phosphate dehydrogenase deficiency enhances germ cell apoptosis and causes defective embryogenesis in Caenorhabditis elegans
has PubMed Central identifier	PMC3674345
has PubMed identifier	23640458
schema:publication	Cell Death Dis
resource representing a document's body	covid:e0187a691be1237e922515d56bcfbc7ec988fa3e#body_text
is http://vocab.deri.ie/void#inDataset of	https://covidontheweb.inria.fr:4443/about/id/http/ns.inria.fr/covid19/e0187a691be1237e922515d56bcfbc7ec988fa3e
is schema:about of	named entity 'P53' named entity 'ALTERED' named entity 'OOGENESIS' named entity 'G6PD' named entity 'HEMOLYTIC ANEMIA' named entity 'HUMAN' named entity 'GLUCOSE' named entity 'ASSOCIATED WITH' named entity 'PMK-1' named entity 'MAPK' named entity 'HYDROGEN PEROXIDE' named entity 'REDUCED' named entity 'C. ELEGANS' named entity 'THESE' named entity 'INDUCED' named entity 'GERM CELL' named entity 'ENHANCED' named entity 'DEFECTIVE' named entity 'PARALLEL' named entity 'PHASE' named entity 'EMBRYONIC LETHALITY' named entity 'G6PD DEFICIENCY' named entity 'G6PD ACTIVITY' named entity '288' named entity 'MITOGEN-ACTIVATED PROTEIN KINASE' named entity 'PHOSPHATE' named entity 'FINDINGS' named entity 'SHORT-TERM' named entity 'INCREASE' named entity 'MICE' named entity 'UPREGULATION' named entity 'mild' named entity 'G6PD deficiency' named entity 'enhanced' named entity 'favism' named entity 'The' named entity 'pathways' named entity 'altered' named entity 'germ cell' named entity 'APOPTOSIS' named entity 'ANIMAL PHYSIOLOGY' named entity 'FULLY' named entity 'HATCHING' named entity 'ANIMAL MODEL' named entity 'H 2' named entity 'KNOWN' named entity 'CAUSES' named entity 'DEHYDROGENASE DEFICIENCY' named entity 'EMBRYOGENESIS' named entity 'CAENORHABDITIS ELEGANS' named entity 'ROLE' named entity 'LOSS OF FUNCTION' named entity 'DID' named entity '2 O' named entity 'DNA' named entity 'DUE TO' named entity 'EGG PRODUCTION' named entity 'AFFECTED' named entity 'EMBRYOGENESIS' named entity 'GERM CELL' named entity 'CAENORHABDITIS ELEGANS' named entity 'RECENTLY' named entity 'ESTABLISHED' named entity 'MUTATION' named entity 'SIGNALING PATHWAYS' named entity 'DEFICIENT' named entity 'NEITHER' named entity 'DEHYDROGENASE' named entity 'DECREASED' named entity 'INVOLVED' named entity 'TO INVESTIGATE'

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