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Transcription profiling of Xenopus hybrid sex reversal experiment

ABSTRACT: This SuperSeries is composed of the following subset Series:; GSE9504: Expression data from hybrid female Xenopus sex reversal experiment; GSE9505: Expression data from hybrid male Xenopus sex reversal experiment Experiment Overall Design: Refer to individual Series

ORGANISM(S): Xenopus laevis x Xenopus muelleri

SUBMITTER: John Malone

PROVIDER: E-GEOD-9507 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Physiological sex predicts hybrid sterility regardless of genotype.

Malone John H JH Michalak P P

Science (New York, N.Y.) 20080101 5859

Reproductive isolation between biological species is characterized by Haldane's rule, which states that the heterogametic sex (XY or ZW) suffers the most dysfunctional effects of hybridization. It has been hypothesized that, in addition to X-linked recessive genes, Haldane's rule also reflects the faster evolution of genes related to male reproduction (faster-male evolution). We used sex-reversed hybrid Xenopus to test faster-male evolution by examining the fertility of sex-reversed individuals ...[more]

PMID: 18174434

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Transcription profiling of Xenopus hybrid femalesex reversal experiment

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Project description:Expression data from hybrid Xenopus sex reversal experiment

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Transcription profiling of Xenopus dorsal root ganglia conditioned in vitro vs freshly dissected control

Project description:Axonal regeneration is enhanced by prior conditioning peripheral nerve lesions. Here we show that Xenopus dorsal root ganglia (DRGs) with attached peripheral nerves (PN-DRGs) can be conditioned in vitro, thereafter showing enhanced axonal growth in response to neurotrophins, similar to preparations conditioned by axotomy in vivo. In contrast to freshly dissected preparations, conditioned PN-DRGs show abundant neurotrophin-induced axonal growth in the presence of actinomycin D, suggesting synthesis of mRNA encoding proteins necessary for axonal elongation occurs during the conditioning period, and this was confirmed by oligonucleotide micro-array analysis.

2008-04-16 | E-MEXP-1297 | biostudies-arrayexpress

Expression data from hybrid male Xenopus sex reversal experiment

Project description:Gene expression was examined in genetic females that were sex-reversed to be phenotypically male compared to normal hybrid males We used microarrays to test expression in the gonad of sex-reversed males (ZW) compared to normal males (ZZ) Keywords: treatment

2007-11-07 | GSE9505 | GEO

Expression data from hybrid female Xenopus sex reversal experiment

Project description:Gene expression was examined in genetic males that were sex-reversed to be phenotypically female compared to normal hybrid females We used microarrays to test expression in the gonad of sex-reversed females (ZZ) compared to normal females (ZW) Keywords: treatment

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Sex reversal following the deletion of a single far upstream enhancer of Sox9.

Project description:Purpose: In this study we employed unbiased, genome wide techniques to identify novel enhancers of Sox9 that may cause Disorders of Sex Development (DSDs) when disrupted in the mouse. Methods: We performed ATAC-seq on 60K FACS-purified gonadal cells before and after sex determination to map nucleosome depleted regions (NDRs) indicative of regulatory elements. We then selected 16 putative enhancers present in Sertoli cells. To determine whether these are active enhancers, we performed ChIP-seq for H3K27ac, a histone modification that marks active enhancers. Transient transgenics was performed on select enhancers to determine whether they drive Sertoli-specific expression in vivo. Finally, we selected a single active Sertoli-specific enhancer to delete with CRISPR. Results: We identified a single enhancer upstream of Sox9 that causes complete male-to-female sex reversal in mice when deleted. Conclusions: Our study is the first to identify a single enhacer supstream of Sox9 which drives Sertoli-specific expression in vivo and causes complete male-to-female sex reversal when deleted in the mouse. Furthermore, this enhancer overlaps a region in humans (XY SR) associated to DSDs.

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