Homology cloning, sequence characterization, and expression analysis of cDNA encoding electron transfer flavoprotein beta polypeptide in mud crab (Scylla paramamosain)

Abstract

ABSTRACT. Electron transfer flavoproteins (ETFs) are αβ-heterodimers found in eukaryotic mitochondria and bacteria. Herein we report a full-length complementary DNA of a mud crab (Scylla paramamosain) ETF β subunit (Scpa-ETFB) isolated with a homology cloning strategy. The complete complementary DNA of the Scpa-ETFB contains a 17-nt 5'-untranslated region, a 765-nt open reading frame encoding 254 amino acids, and a 248-nt 3'-untranslated region. The high identity of Scpa-ETFB with ETFB in other organisms indicated that Scpa-ETFB is a new member of the ETFB family. Although the conserved motif associated with flavin adenine dinucleotide binding is absent in Scpa-ETFB, the signature sequences of the ETF superfamily were identified. Using reverse transcriptase polymerase chain reaction, we detected the messenger RNA transcript of Scpa-ETFB in high levels in the tissues of the hepatopancreas, ovary, heart, and muscle. Phylogenetic analysis showed that Scpa-ETFB is most closely related to the ETFB genes of Caligus rogercresseyi and Lepeophtheirus salmonis. These results provided basic information for elucidating the molecular mechanism of energy production in the mud crab.

Repression of let‐7b‐5p prevents the development of multifidus muscle dysfunction by promoting vitamin D accumulation via upregulation of electron transfer flavoprotein alpha subunit in a rat model of multifidus muscle injury

“…We proved that ETFA, a target gene of let‐7b‐5p, is negatively regulated by let‐7b‐5p, indicating that let‐7b‐5p associated functions of multifidus muscle dysfunction might be associated with ETFA. ETFA, a member of ETFs, are αβ‐heterodimers that involved in the eukaryotic mitochondria and the bacteria . Novel ETF dehydrogenase mutations were reported to affect patients suffering from a deficiency of mild glutaric aciduria type II and complex II‐III in muscle and liver by regulating mild fat infiltration .…”

“…ETFA, a member of ETFs, are αβ-heterodimers that involved in the eukaryotic mitochondria and the bacteria. 30 Novel ETF dehydrogenase mutations were reported to affect patients suffering from a deficiency of mild glutaric aciduria type II and complex II-III in muscle and liver by regulating mild fat infiltration. 31 ETFDH gene mutations together with the secondary mitochondrial proliferation could elevate muscle coenzyme Q10 in riboflavin-responsive multiple acyl-coenzyme a dehydrogenation deficiency, 32 indicating that ETFA gene may be involved in muscle-related disease.…”