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Abrogation of MAP4K4 protein function causes congenital anomalies in humans and zebrafish
Journal article   Open access   Peer reviewed

Abrogation of MAP4K4 protein function causes congenital anomalies in humans and zebrafish

Victoria Patterson, Farid Ullah, Laura Bryant, John N. Griffin, Alpa Sidhu, Sheila Saliganan, Mackenzie Blaile, Margarita S. Saenz, Rosemarie Smith, Sara Ellingwood, …
Science advances, Vol.9(17), eade0631
04/26/2023
DOI: 10.1126/sciadv.ade0631
PMCID: PMC10132768
PMID: 37126546
url
https://doi.org/10.1126/sciadv.ade0631View
Published (Version of record) Open Access

Abstract

We report 21 families displaying neurodevelopmental differences and multiple congenital anomalies while bearing a series of rare variants in mitogen-activated protein kinase kinase kinase kinase 4 ( MAP4K4 ). MAP4K4 has been implicated in many signaling pathways including c-Jun N-terminal and RAS kinases and is currently under investigation as a druggable target for multiple disorders. Using several zebrafish models, we demonstrate that these human variants are either loss-of-function or dominant-negative alleles and show that decreasing Map4k4 activity causes developmental defects. Furthermore, MAP4K4 can restrain hyperactive RAS signaling in early embryonic stages. Together, our data demonstrate that MAP4K4 negatively regulates RAS signaling in the early embryo and that variants identified in affected humans abrogate its function, establishing MAP4K4 as a causal locus for individuals with syndromic neurodevelopmental differences. MAP4K4 variants abrogate its negative regulation of RAS signaling, causing neurodevelopmental differences in 21 families.
Genetics Biomedicine and Life Sciences Human Genetics SciAdv r-articles

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