Project description:Several mechanisms have been proposed to account for Sdh-mutation-induced tumorigenesis, the most accepted of which is based on the constitutive expression of the hypoxia-inducible factor 1alpha (Hif1alpha) at normal oxygen tension, a theory referred to as pseudo-hypoxic drive. Other molecular processes, such as oxidative stress, apoptosis or chromatin remodeling have been also proposed to play a causative role. Nevertheless, the actual contribution of each of these mechanisms has not been definitively established. Moreover, the biological factors that determine the tissue-specificity of these tumors have not been identified. In this work, we made use of the inducible SDHD-ESR mouse, a conditional mutant in the SdhD gene, which encodes the small subunit of MCII, and that acts as a tumor suppressor gene in humans. We performed microarray analysis of kidney in order to identify other early gene expression changes elicited by SdhD deletion. 8 samples from heterozygous (+/-) and 8 samples from null mutants (SDHD-ESR), paired by two and hybrydized against a pool of 8 samples from homozygous wt (+/+) animals.
Project description:SILAC based protein correlation profiling using size exclusion of protein complexes derived from Mus musculus tissues (Heart, Liver, Lung, Kidney, Skeletal Muscle, Thymus)
Project description:SILAC based protein correlation profiling using size exclusion of protein complexes derived from seven Mus musculus tissues (Heart, Brain, Liver, Lung, Kidney, Skeletal Muscle, Thymus)
Project description:Several mechanisms have been proposed to account for Sdh-mutation-induced tumorigenesis, the most accepted of which is based on the constitutive expression of the hypoxia-inducible factor 1alpha (Hif1alpha) at normal oxygen tension, a theory referred to as pseudo-hypoxic drive. Other molecular processes, such as oxidative stress, apoptosis or chromatin remodeling have been also proposed to play a causative role. Nevertheless, the actual contribution of each of these mechanisms has not been definitively established. Moreover, the biological factors that determine the tissue-specificity of these tumors have not been identified. In this work, we made use of the inducible SDHD-ESR mouse, a conditional mutant in the SdhD gene, which encodes the small subunit of MCII, and that acts as a tumor suppressor gene in humans. We performed microarray analysis of adrenal medulla (AM) in order to identify other early gene expression changes elicited by SdhD deletion. 8 samples from heterozygous (+/-) and 8 samples from null mutants (SDHD-ESR), paired by two and hybrydized against a pool of 8 samples from homozygous wt (+/+) animals.
Project description:Several mechanisms have been proposed to account for Sdh-mutation-induced tumorigenesis, the most accepted of which is based on the constitutive expression of the hypoxia-inducible factor 1alpha (Hif1alpha) at normal oxygen tension, a theory referred to as pseudo-hypoxic drive. Other molecular processes, such as oxidative stress, apoptosis or chromatin remodeling have been also proposed to play a causative role. Nevertheless, the actual contribution of each of these mechanisms has not been definitively established. Moreover, the biological factors that determine the tissue-specificity of these tumors have not been identified. In this work, we made use of the inducible SDHD-ESR mouse, a conditional mutant in the SdhD gene, which encodes the small subunit of MCII, and that acts as a tumor suppressor gene in humans. We performed microarray analysis of kidney in order to identify other early gene expression changes elicited by SdhD deletion.
Project description:We collected whole genome testis expression data from hybrid zone mice. We integrated GWAS mapping of testis expression traits and low testis weight to gain insight into the genetic basis of hybrid male sterility.