ArticleGenetics1999
The primary sex determination signal of Caenorhabditis elegans.
Article in Genetics, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
14 citing papers in PubMed, 27 citations in OpenAlex.
- Small RNA-mediated genetic switches coordinate ALG-3/4 small RNA pathway function.Nucleic acids research · 2024Article
- XOL-1 regulates developmental timing by modulating the H3K9 landscape in C. elegans early embryos.PLoS genetics · 2024Article
- Chromatin Organization duringDNA · 2024Article
- Review
- Transcription Factors That Control Behavior-Lessons FromFrontiers in neuroscience · 2021Review
- Dose-dependent action of the RNA binding protein FOX-1 to relay X-chromosome number and determineeLife · 2020Article
- Evidence that metabolism and chromosome copy number control mutually exclusive cell fates in Bacillus subtilis.The EMBO journal · 2011Article
- Restricting dosage compensation complex binding to the X chromosomes by H2A.Z/HTZ-1.PLoS genetics · 2009Article
- The worm solution: a chromosome-full of condensin helps gene expression go down.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2009Article
- Article
- Article
- The T-box transcription factor SEA-1 is an autosomal element of the X:A signal that determines C. elegans sex.Developmental cell · 2005Article
- Molecular correlates of genes exhibiting RNAi phenotypes in Caenorhabditis elegans.Genome research · 2003Article
- Exploring the envelope. Systematic alteration in the sex-determination system of the nematode caenorhabditis elegans.Genetics · 2002Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
An X chromosome counting process determines sex in Caenorhabditis elegans. The dose of X chromosomes is translated into sexual fate by a set of X-linked genes that together control the activity of the sex-determination and dosage-compensation switch gene, xol-1. The double dose of X elements in XX animals represses xol-1 expression, promoting the hermaphrodite fate, while the single dose of X elements in XO animals permits high xol-1 expression, promoting the male fate. Previous work has revealed at least four signal elements that repress xol-1 expression at two levels, transcriptional and post-transcriptional. The two molecularly characterized elements include an RNA binding protein and a nuclear hormone receptor homolog. Here we explore the roles of the two mechanisms of xol-1 repression and further investigate how the combined dose of X signal elements ensures correct, sex-specific expression of xol-1. By studying the effects of increases and decreases in X signal element dose on male and hermaphrodite fate, we demonstrate that signal elements repress xol-1 cumulatively, such that full repression of xol-1 in XX animals results from the combined effect of individual elements. Complete transformation from the hermaphrodite to the male fate requires a decrease in the dose of all four elements, from two copies to one. We show that both mechanisms of xol-1 repression are essential and act synergistically to keep xol-1 levels low in XX animals. However, increasing repression by one mechanism can compensate for loss of the other, demonstrating that each mechanism can exert significant xol-1 repression on its own. Finally, we present evidence suggesting that xol-1 activity can be set at intermediate levels in response to an intermediate X signal.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.