13578_2022_917_MOESM1_ESM.tif (2.78 MB)
Additional file 1 of The balance between NANOG and SOX17 mediated by TET proteins regulates specification of human primordial germ cell fate
figure
posted on 2022-11-05, 16:25 authored by Zili Li, Fang Fang, Yuting Long, Qian Zhao, Xiaotong Wang, Zhen Ye, Tianqing Meng, Xiuli Gu, Wenpei Xiang, Chengliang Xiong, Honggang LiAdditional file 1: Fig. S1. Generation of TET Gene Knockout hESC Lines, Related to Fig. 1. (A) Design of the CRISPR targets for TET genes, using gRNAs (red arrows) that target the sequences corresponding to the beginning of the catalytic domain in TET1, TET2 and TET3; (B) The efficiency for the homozygous knockouts of the TET alleles. The knockouts (KO) were confirmed as bi-allelic frame-shift nonsense mutations. The others include wild-types or heterozygous mutants, or alleles with deletions/insertions of 3 × N base pairs; (C) The DNA sequences of both alleles for the indicated knockout lines. Red letters indicate the positions of the guide RNAs. del: deletion; ins: insertion; (D) Sanger sequencing of TKO hESCs in TET gene target locus.
History
Usage metrics
Categories
Keywords
time quantitative pcrgenome bisulfite sequencinginvolved signaling pathwaysundergo epigenetic reprogrammingrescued hpgclc inductioninhibited hpgclc inductionkey genes playsnodal signaling pathwaysox17 promoters repressednanog could bindmeasure gene expressionglobal mrna transcriptionimpeded hpgc specificationdna methylation profilesearly hpgc specificationtet proteins knockoutnodal signalinghpgc specificationhpgc inductiondna methylationearly postinduced hpgctet proteinsrelated genesnanog proteinsmediated methylationdownstream geneshpgclcs specificationhpgclcs inductionwestern blottet3 triplesox17 promotersox17 mediatedsox17 expressionregulatory mechanismprotein levelspluripotent cellsnovel functionmkate2 reportermethylcytosine modulatesmediated oxidationmediated hypermethylationlines bearinglike cellsimplantation embryogastrulation failurefundamental roleepigenetic balance
Licence
Exports
RefWorks
BibTeX
Ref. manager
Endnote
DataCite
NLM
DC