ArticleGenetics2002
A haplolethal locus uncovered by deletions in the mouse T complex.
Article in Genetics, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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.
The trial behind it
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
9 citing papers in PubMed, 14 citations in OpenAlex.
- Dissection of a Down syndrome-associated trisomy to separate the gene dosage-dependent and -independent effects of an extra chromosome.Human molecular genetics · 2023Article
- The haplolethality paradox of the wupA gene in Drosophila.PLoS genetics · 2021Article
- Interallelic and intergenic incompatibilities of the Prdm9 (Hst1) gene in mouse hybrid sterility.PLoS genetics · 2012Article
- Creating a "hopeful monster": mouse forward genetic screens.Methods in molecular biology (Clifton, N.J.) · 2011Article
- PDCD2 is essential for inner cell mass development and embryonic stem cell maintenance.Developmental biology · 2010Article
- Conserved alternative and antisense transcripts at the programmed cell death 2 locus.BMC genomics · 2007Article
- Transgenic rescue of the mouse t complex haplolethal locus Thl1.Mammalian genome : official journal of the International Mammalian Genome Society · 2005Article
- X-ray-induced deletion complexes in embryonic stem cells on mouse chromosome 15.Mammalian genome : official journal of the International Mammalian Genome Society · 2005Article
- Overlapping deletions spanning the proximal two-thirds of the mouse t complex.Mammalian genome : official journal of the International Mammalian Genome Society · 2003Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Proper levels of gene expression are important for normal mammalian development. Typically, altered gene dosage caused by karyotypic abnormalities results in embryonic lethality or birth defects. Segmental aneuploidy can be compatible with life but often results in contiguous gene syndromes. The ability to manipulate the mouse genome allows the systematic exploration of regions that are affected by alterations in gene dosage. To explore the effects of segmental haploidy in the mouse t complex on chromosome 17, radiation-induced deletion complexes centered at the Sod2 and D17Leh94 loci were generated in embryonic stem (ES) cells. A small interval was identified that, when hemizygous, caused specific embryonic lethal phenotypes (exencephaly and edema) in most fetuses. The penetrance of these phenotypes was background dependent. Additionally, evidence for parent-of-origin effects was observed. This genetic approach should be useful for identifying genes that are imprinted or whose dosage is critical for normal embryonic development.
Indexed as
Identifiers
What OpenQuestion holds
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.