Genome-wide analysis of FSH and LH dependent gene expression and the crosstalk between these two pathways in mice testes
Ontology highlight
ABSTRACT: Effects of the absence of a functional LH receptor and/or expression of a constitutively active FSH receptor on gene expression in the gonads of male mice were studied. The results provide insights into the roles of the hormones LH and FSH in male reproduction. The main conclusion is that constant strong FSH stimulation is able to rescue the impaired spermatogenesis and fertility of male mice in the absence of LH signalling. Total RNA was obtained from testis of 12 weeks old mice of different genotypes and extracted using Trizol followed by clean up with Qiage RNeasy MinElute Cleanup Kit
Project description:Effects of lack of functional LH receptor and/or a constitutively active FSH receptor on gene expression in the ovaries of female mice were studied. The results suggest that transgenic expression of the mouse Fshr in granulosa cells leads to abnormal ovarian structure/function and infertility. This finding indicates that gain-of-function mutations of the Fshr in female mice bring about distinct and clear changes in ovarian function. Total RNA was obtained from ovaries of 12 weeks old mice of different genotypes and extracted using Trizol followed by clean up with Qiage RNeasy MinElute Cleanup Kit
Project description:in 25% - 30% of all OS cases the chromosome region 17p11.2-p12 is aberrant. Using SNP array in conjunction with expression microarrays we try to identify genes which can be classified as oncogens or are in someway benificial to the survival of the tumor. To identify minimal significant amplified region(s) that is(are) aberrant in osteosarcoma tumorigenesis, with a special emphasis on but not limitied to chromosome region 17p11.2-p12
Project description:Mechanisms of neuroendocrine tumor (NET) proliferation are poorly understood and therapies that effectively control NET progression and metastatic disease are limited. We found amplification of a putative oncogene, RABL6A, in primary human pancreatic NETs (PNETs) that correlated with high level RABL6A protein expression. Consistent with those results, stable silencing of RABL6A in cultured BON-1 PNET cells revealed that it is essential for their proliferation and survival. Cells lacking RABL6A predominantly arrested in G1 phase with a moderate mitotic block. Pathway analysis of microarray data suggested activation of the p53 and retinoblastoma (Rb1) tumor suppressor pathways in the arrested cells. Specific inactivation of p53 had no effect on the RABL6A knockdown phenotype, indicating RABL6A functions independent of p53 in this setting. By comparison, Rb1 inactivation restored G1 to S phase progression in RABL6A knockdown cells although it was insufficient to override the mitotic arrest and cell death caused by RABL6A loss. Thus, RABL6A promotes G1 progression in PNET cells by inactivating Rb1, an established suppressor of PNET proliferation and development. This work identifies RABL6A as a new negative regulator of Rb1 that is essential for PNET proliferation and survival. We suggest RABL6A is a new potential biomarker and target for anticancer therapy in PNET patients. Total RNA obtained from human BON-1 PNET cells with RABL6A shRNA knockdown compared to BON-1 cells expressing control vector.
Project description:TRPM7 is a ubiquitous ion channel and kinase, a unique M-bM-^@M-^XchanzymeM-bM-^@M-^Y, required for proper early embryonic development. In order to assess the effects of TRPM7 activity on cellular gene expression, mouse embryonic stem cells with TRPM7 gene deletion (TRPM7-/- mESC) were established. By using microarray analysis, we identified genes with transcription significantly different in TRPM7-deficient mESC. Total RNA was extracted from cells using Qiagen RNAeasy Plus mini Kit. Triplicate samples were made for each wild type clone 3 (WT3) and and TRPM7-/- clone 9 (KO9) mESC
Project description:In this study, we screened a cohort of 57 paediatric brain tumours, with a wide range of pathologies to identify microRNA profiles We analysed the microRNA profiles in paediatric brain tumours as compared to normal adult brain. Our cohort included 14 pilocytic astrocytomas, 3 diffuse astrocytomas, 2 anaplastic astrocytomas, 5 glioblastomas, 14 ependymomas, 9 medulloblastomas, 5 atypical teratoid/rhabdoid tumours, 4 choroid plexus papillomas, 1 papillary glioneuronal, and 7 adult brain controls.
Project description:In this study, we screened a cohort of 57 paediatric brain tumours, with a wide range of pathologies to identify gene expression profiles We analysed gene expression in paediatric brain tumours as compared to normal adult brain in order to understand the molecular profiles. Our cohort included 15 pilocytic astrocytomas, 3 diffuse astrocytomas, 2 anaplastic astrocytomas, 5 glioblastomas, 14 ependymomas, 9 medulloblastomas, 5 atypical teratoid/rhabdoid tumours, 4 choroid plexus papillomas, 8 adult brain and 8 foetal brain controls.
Project description:Genome-wide association studies (GWASs) identified the MEIS1 locus for Restless Legs Syndrome (RLS), but causal single nucleotide polymorphisms (SNPs) and the functional relevance have remained to be elucidated. The MEIS1 locus contains an exceptionally large number of highly conserved non-coding regions (HCNRs), which potentially function as cis-regulatory modules. We analyzed the HCNRs in the RLS-associated linkage disequilibrium (LD) block for allele-dependent enhancer activity in both zebrafish and mouse, comparing the protective and risk alleles of RLS-associated common variants. We found one enhancer, harboring the lead SNP rs12469063, which showed an allele-dependent reduction of reporter gene expression exclusively in the embryonic ganglionic eminences at developmental stage E12.5. Notably, the reporter activity overlapped with the endogenous telencephalic Meis1 expression domain, which co-localized with transcripts of all four validated RLS loci. Thus, the developing telencephalon represents the first neuroanatomic region implicated for RLS based on GWAS findings. Total RNA obtained from 2-3 male and female mice E12.5 (wildtype, heterzygote, homozygote) and 3-4 male heterozygote and wildtype mice (adult)
Project description:Analysis of differential gene expression in Psen-null and RBPjk-null epidermal keratinocytes. The hypothesis tested in the present study was that canonical Notch signals could be present at the beginning of epidermal stratification (E13.5) in the RBPj-null epidermis. If an early signal was preserved by epigenetic memory, E18.5 RBPj-null epidermis would resemble the wild-type at the transcriptional level. Total RNA obtained from 3xRBPj-null and 3xPsen-null epidermis at E18.5 and compared to wild-type (3xRBPjwt & 3xPsenwt) epidermis from littermates.