FN Archimer Export Format
PT J
TI An epigenetic molluscicide
BT 
AF Luviano, Nelia
   Halby, Ludovic
   Jallet, Corinne
   Arimondo, Paola B.
   Cosseau, Celine
   Grunau, Christoph
AS 1:1;2:2;3:2;4:2;5:1;6:1;
FF 1:;2:;3:;4:;5:;6:;
C1 IHPE, Univ Perpignan Via Domitia, CNRS, IFREMER, Univ Montpellier, Perpignan, France
   Epigenetic Chemical Biology, Department of Structural Biology and Chemistry, Institut Pasteur, Université de Paris-Cité, UMR n°3523, CNRS, 28 Rue du Dr Roux, Paris 75015, France
C2 UNIV PERPIGNAN, FRANCE
   INST PASTEUR, FRANCE
UM IHPE
TC 0
UR https://archimer.ifremer.fr/doc/00847/95926/103872.pdf
LA English
DT Article
DE ;schistosomiases;Biomphalaria glabrata;molluscicide;epigenetics;DNA methylation inhibitor
AB Biomphalaria glabratais a fresh-water mollusk that serves as obligatory intermediate host toSchistosoma mansoni, agent of the neglected tropical disease schistosomiasis that affects roughly 250 Mio people. One of the ways to control the pathogenic agent is to interrupt the life cycle by eliminating the intermediate snail host though foal treatment of water bodies with molluscicides. Currently recommended molluscicides were developed in the 1950ths and lack sufficient specificity, e.g., they are toxic to fish. To provide new lead compounds for the development of a new type of molluscicides we used a rational approach based on the hypotheses that interfering with an important epigenetic mark, DNA methylation, would impede development of the snail host. We present here the compound 29, analogues-based compound that mimic substrates of DNA methyltransferases. We show that compound 29 has (i) low cytotoxicity for human cells, (ii) it inhibits DNA methylation, and (iii) it decreases fecundity inB.glabrata. It is therefore conceivable to produce compounds that act as specific epigenetic molluscicides. 
PY 2023
PD MAR
SO bioRxiv
PU Cold Spring Harbor Laboratory
DI 10.1101/2023.03.21.533666
ID 95926
ER

EF