Correction:Knockout of lipoprotein lipase with CRISPR/Cas9 causes severe developmental defects and affects lipid deposition in Japanese medaka(Oryzias latipes)

There are some errors in Fig.4 and it needs to be corrected(Feng and Liang,2022).The Oil Red O staining results of the two groups of the muscle calculated previously were false positive,and the correct results should be"not detected(ND)",which needs to be corrected in Fig.4G.

Transcriptional responses of mu-, pi- and omega-class glutathione S-transferase genes in the hepatopancreas of Cipangopaludina cahayensis exposed to microcystin-LR

The glutathione S-transferases(GSTs)play important roles in detoxification of microcystins(MCs),but the responses of GSTs to MC-LR have not been well characterized in freshwater gastropod,Cipangopaludina cahayensis.In the present study,we cloned full-length cDNAs of mu-and pi-class GSTs(GSTM and GSTP)and partial cDNA of omega-class GST(GSTO),and determined the transcriptional responses of the three GST genes to different concentrations of MC-LR(0,1,10 and 100 lg/L)in C.cahayensis.The full-length cDNAs of GSTM and GSTP of C.cahayensis were 813 and 820 bp,containing an open reading frame(ORF)of 648 bp(encoding 215 amino acids)and 624 bp(encoding 207 amino acids),respectively.The mRNA expression of GSTM and GSTO significantly decreased after exposure to 10 lg/L MC-LR,and the mRNA expression of GSTP significantly decreased after100 lg/L MC-LR exposure.This might contribute to the detoxication of MCs in C.cahayensis,which is consistent with its sedentary life and filter-feeder status.The mRNA expression of the three GST isoforms in C.cahayensis could be used as biomarkers for water contamination.

Knockout of lipoprotein lipase with CRISPR/Cas9 causes severe developmental defects and affects lipid deposition in Japanese medaka(Oryzias latipes)

In mammals,lipoprotein lipase(LPL)has been found to play an important role in lipid mentalismand deposition.LPL deficiency in humans(Homo sapiens)and mice(Mus musculus)tends to cause hypertriglyceridemia.The lpl gene is not expressed in adult mammalian liver,but is in adult fish liver.The functions provided by the lpl gene are diverse in vertebrates.Here,we knocked out the lpl gene in Japanese medaka(Oryzias latipes)with the CRISPR/Cas9 system.The lpl-knockout(KO)homozygous individuals showed severe developmental defects with an extremely emaciated and deformedbody and onlyaccounted for about5%of the F2fish.This is consistentwiththefindings inmicebut disaccords with the results for zebrafish(Danio rerio).Compared with wild-type(WT)madaka,the mRNA level of lpl in lpl-KO heterozygous mutant was significantly higher in the muscle,showed no significant difference in the liver,and was significantly lower in the heart.Under lpl heterozygous deficiency,the relative area of Oil RedO and triglycerides(TG)level in the liver,heart and muscle tissue covaried with levels of lpl mRNA in medaka.The lpl heterozygous deficiency did not affect the levelsofTG,low-density lipoprotein cholesterol(LDL-C),high-density lipoprotein cholesterol(HDL-C)and total cholesterol(TC)in the plasma of medaka,which is inconsistent with the findings in mammals.In general,the lpl gene plays an important role in the growth and development and is closely related to lipid deposition of medaka.