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This facilitate large-scale mapping of zebrafish estrogen-responsive genes to the corresponding human homologs.
Furthermore this work validates the usefulness of our methodology for rapid, systematic and inexpensive microsatellite mapping of zebrafish mutations.
In addition, the genomic locations of all 29 genes have been found, allowing rapid candidate gene discovery during genetic mapping of zebrafish dystrophy mutants.
We have obtained rough map positions for over 300 zebrafish mutants with an accuracy of approximately 6 cM and thereby validated the usefulness of our methodology for rapid, systematic and inexpensive microsatellite mapping of zebrafish mutations.
Therefore, the aims of the study were to achieve a comprehensive mapping of zebrafish hepatic proximal promoter CGI methylation in both normal liver and in chemically induced hepatocellular carcinoma (HCC) tumors.
These data should aid in the genetic mapping of zebrafish dystrophy mutants, creation of mutant lines for high-throughput testing of dystrophy therapies, and identification of novel dystrophy-causing genes.
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This led to the development of the first 3-D trace map of zebrafish locomotor behaviors in response to drug treatment.
Seven RH maps have been reported in six teleost fishes, including two maps of zebrafish [ 26, 27], gilthead sea bream [ 28], medaka [ 29], European sea bass [ 30], Nile tilapia [ 31] and yellowtail [ 32].
As a paralogous relationship between zebrafish chromosomes 1 and 11 has not been reported so far and since there are frequent discrepancies between mapping data of zebrafish genes and their chromosomal assignment in current genome assemblies ([ 35] and own observations), we mapped tyrp1a using the radiation hybrid panel LN54 [ 36].
We thank A. Bohnert for the physical mapping of the zebrafish slc1 genes and Corinne Hodel and Dr. Edda Kastenhuber for critical reading of the manuscript.
Positioning these genes allows rapid candidate identification during genetic mapping of dystrophic zebrafish mutants and may allow prioritization of novel mutants – those with linkage to a genomic region containing no known dystrophy-associated ortholog.
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