Identification and characterization of Laodelphax striatellus (Insecta: Hemiptera: Delphacidae) neutral sphingomyelinase

Abstract

The neutral sphingomyelinase (nSMase) 1 homologue gene LsSMase was cloned from Laodelphax striatellus, a direct sap-sucker and virus vector of gramineous plants, and expressed via a Bac to Bac baculovirus expression system. The LsSMase-enhanced green fluorescent protein fusion protein was located in the endoplasmic reticulum in a similar manner to mammalian nSMase 1. The biochemical properties of LsSMase were determined in detail. The optimal pH and temperature for recombinant LsSMase were 8 and 37 °C, respectively. LsSMase was an Mg or Mn dependent enzyme, but different concentration of each were needed. The activity of LsSMase was significantly stimulated by Ethylene glycol bis(2-aminoethyl ether)tetraacetic acid (EGTA), whereas it was inhibited by ethylenediaminetetraacetic acid. Millimolar concentrations of Zn completely inhibited LsSMase. The reducing agents dithiothreitol and β-mercaptoethanol varied in their effects on activity. Phospholipids were not found to stimulate LsSMase.

The cellular and molecular origins of extracellular vesicles released by the helminth pathogen, Fasciola hepatica

“…Indeed, treating FhEVs with GW4869 inhibited FhEVassociated neutral SMase activity in a dose-dependent manner. However, residual activity following GW4869 treatment suggests that FhSMPD2 may be refractory to this inhibitor (compared to human enzymes) as has been reported for insect SMase (Zhou et al 2017).…”

Knockdown of sphingomyelinase (NlSMase) causes ovarian malformation of brown planthopper,Nilaparvata lugens(Stål)

“…The sphingomyelinase (SMPD) of Bombus lantschouensis , which was highly expressed in the ovary and pupa of the queen bee, mediated the pupa development (Han et al, 2017; Han et al, 2018). One neutral SMase ( LsSMase ) was reported in Laodelphax striatellus and showed the highest expression in the ovary in female adults (Zhou et al, 2017). Moreover, it had been reported that the disruption of sphingolipid metabolism elicited reproductive defects in Drosophila (Guo et al, 2014).…”