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Zebrafish knockout of Down syndrome gene, DYRK1A, shows social impairments relevant to autism

Overview of attention for article published in Molecular Autism, September 2017
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About this Attention Score

  • Above-average Attention Score compared to outputs of the same age (64th percentile)

Mentioned by

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2 tweeters
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2 patents

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144 Mendeley
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Title
Zebrafish knockout of Down syndrome gene, DYRK1A, shows social impairments relevant to autism
Published in
Molecular Autism, September 2017
DOI 10.1186/s13229-017-0168-2
Pubmed ID
Authors

Oc-Hee Kim, Hyun-Ju Cho, Enna Han, Ted Inpyo Hong, Krishan Ariyasiri, Jung-Hwa Choi, Kyu-Seok Hwang, Yun-Mi Jeong, Se-Yeol Yang, Kweon Yu, Doo-Sang Park, Hyun-Woo Oh, Erica E. Davis, Charles E. Schwartz, Jeong-Soo Lee, Hyung-Goo Kim, Cheol-Hee Kim

Abstract

DYRK1A maps to the Down syndrome critical region at 21q22. Mutations in this kinase-encoding gene have been reported to cause microcephaly associated with either intellectual disability or autism in humans. Intellectual disability accompanied by microcephaly was recapitulated in a murine model by overexpressing Dyrk1a which mimicked Down syndrome phenotypes. However, given embryonic lethality in homozygous knockout (KO) mice, no murine model studies could present sufficient evidence to link Dyrk1a dysfunction with autism. To understand the molecular mechanisms underlying microcephaly and autism spectrum disorders (ASD), we established an in vivo dyrk1aa KO model using zebrafish. We identified a patient with a mutation in the DYRK1A gene using microarray analysis. Circumventing the barrier of murine model studies, we generated a dyrk1aa KO zebrafish using transcription activator-like effector nuclease (TALEN)-mediated genome editing. For social behavioral tests, we have established a social interaction test, shoaling assay, and group behavior assay. For molecular analysis, we examined the neuronal activity in specific brain regions of dyrk1aa KO zebrafish through in situ hybridization with various probes including c-fos and crh which are the molecular markers for stress response. Microarray detected an intragenic microdeletion of DYRK1A in an individual with microcephaly and autism. From behavioral tests of social interaction and group behavior, dyrk1aa KO zebrafish exhibited social impairments that reproduce human phenotypes of autism in a vertebrate animal model. Social impairment in dyrk1aa KO zebrafish was further confirmed by molecular analysis of c-fos and crh expression. Transcriptional expression of c-fos and crh was lower than that of wild type fish in specific hypothalamic regions, suggesting that KO fish brains are less activated by social context. In this study, we established a zebrafish model to validate a candidate gene for autism in a vertebrate animal. These results illustrate the functional deficiency of DYRK1A as an underlying disease mechanism for autism. We also propose simple social behavioral assays as a tool for the broader study of autism candidate genes.

Twitter Demographics

The data shown below were collected from the profiles of 2 tweeters who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 144 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 144 100%

Demographic breakdown

Readers by professional status Count As %
Student > Bachelor 29 20%
Student > Master 23 16%
Student > Ph. D. Student 21 15%
Researcher 12 8%
Student > Doctoral Student 7 5%
Other 24 17%
Unknown 28 19%
Readers by discipline Count As %
Neuroscience 24 17%
Biochemistry, Genetics and Molecular Biology 22 15%
Psychology 16 11%
Agricultural and Biological Sciences 12 8%
Medicine and Dentistry 11 8%
Other 21 15%
Unknown 38 26%

Attention Score in Context

This research output has an Altmetric Attention Score of 4. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 01 July 2021.
All research outputs
#6,491,901
of 21,453,375 outputs
Outputs from Molecular Autism
#452
of 646 outputs
Outputs of similar age
#102,357
of 297,349 outputs
Outputs of similar age from Molecular Autism
#1
of 1 outputs
Altmetric has tracked 21,453,375 research outputs across all sources so far. This one has received more attention than most of these and is in the 69th percentile.
So far Altmetric has tracked 646 research outputs from this source. They typically receive a lot more attention than average, with a mean Attention Score of 28.7. This one is in the 29th percentile – i.e., 29% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 297,349 tracked outputs that were published within six weeks on either side of this one in any source. This one has gotten more attention than average, scoring higher than 64% of its contemporaries.
We're also able to compare this research output to 1 others from the same source and published within six weeks on either side of this one. This one has scored higher than all of them