GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE222nnn/GSE222656/primaryOK200TranscriptomicsMus musculus Genome binding/occupancy profiling by high throughput sequencingExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE222656GEOGSEfalseRNA-seq and Cut & Tag analyses of mouse 2-cell embryos in which lamin B1 dissociation from the nuclear envelope is inhibitedWe have found that lamin B1 is dissociated from the nuclear envelope transiently at the 2-cell stage during mouse embryonic development. This lamin B1 dissociation is mediated by autophagy and can be inhibited by interfering with lamin B1’s binding to LC3, a factor responsible for early autophagosome formation. In order to block interaction between lamin B1 and LC3, we injected mRNA harboring the LC3-binding domain of lamin B1 to mouse embryos and examined transcriptomes of the injected embryos by RNA sequencing (RNA-seq) analysis. In addition, embryos expressed with full-length lamin B1 mRNA harboring two different types of mutations (flLB1(F454A/L457A) and flLB1(5A)) were analyzed by RNA-seq, together with non-injection control (Non2). Another injection control (flLB1(F454A/L457A)ΔC) was also performed, together with a non-injection control (Non3). Furthermore, the effect of nuclear stiffening was examined by expressing the molecular tether-anchor system (tWT), together with a mutant carrying LaG165A (tMut) and a non-injection control (Non4). Chromatin states of such embryos were analyzed by Cut & Tag using anti-H3K4me3 antibody.2026/08/08GSE222656GSM9843101GSM8599434GSM9843102GSM9843103GSM9843104GSM9843105GSM8599439GSM9843106GSM9843107GSM9843108GSM9843109GSM8599435GSM8599436GSM8599438GSM6928376GSM6928377GSM6928378GSM6928379GSM8599442GSM9843110GSM8599443GSM9843111GSM8599444GSM9843112GSM8599445GSM9843113GSM9843114GSM8599440GSM9843115GSM8599446GSM8599447GSM8599448GSM6928387GSM6928380GSM6928381GSM6928382GSM6928383GSM6928384GSM6928385GSM69283862845730172222656Mus musculus