Bulk RNA-seq of multiple organs in LmnaG609G progeria mice with inducible ?133p53a
Hutchinson–Gilford progeria syndrome (HGPS) is a premature aging disorder caused by LMNA mutations that produce progerin. To investigate whether the senescence-inhibitory human p53 isoform ?133p53a counteracts progeroid phenotypes in vivo, we generated mice carrying a Cre/loxP-inducible ?133p53a transgene and crossed them with LmnaG609G mice. Bulk RNA-seq was performed on heart, kidney, liver, and skeletal muscle from wild-type and LmnaG609G/+ mice across five experimental groups. Transcriptomes were analyzed to identify ?133p53a-associated gene expression programs and pathway-level changes across organs. This dataset provides a multi-organ resource to interrogate transcriptional signatures linked to ?133p53a induction in a progeria model and support mechanistic interpretation of the associated manuscript. Overall design: Bulk RNA-seq was performed on heart, kidney, liver, and skeletal muscle collected from 9–10-month-old mice (n = 5 per tissue per group (4 in kidney); total n = 99). The dataset includes five groups: a wild-type group lacking the LmnaG609G allele (Lmna^+/+) and four groups on the heterozygous progeria background (Lmna^G609G/+) defined by a Cre/loxP-inducible human ?133p53a transgene and tamoxifen exposure as follows: Group-1, CAG-133^Tam/+;Cre^Tg/+;Lmna^G609G/+ injected with tamoxifen at 5–6 weeks of age; Group-2, CAG-133^LSL/+;Cre^Tg/+;Lmna^G609G/+ without tamoxifen injection; Group-3, CAG-133^+/+;Cre^Tg/+;Lmna^G609G/+ injected with tamoxifen at 5–6 weeks of age; and Group-4, CAG-133^+/+;Cre^+/+;Lmna^G609G/+ without tamoxifen injection. Reads were processed to generate gene-level expression matrices for differential expression and pathway analyses.