PUBLICATION

Limb body wall complex, amniotic band sequence, or new syndrome caused by mutation in IQ Motif containing K (IQCK)?

Authors
Kruszka, P., Uwineza, A., Mutesa, L., Martinez, A.F., Abe, Y., Zackai, E.H., Ganetzky, R., Chung, B., Stevenson, R.E., Adelstein, R.S., Ma, X., Mullikin, J.C., Hong, S.K., Muenke, M.
ID
ZDB-PUB-151006-9
Date
2015
Source
Molecular genetics & genomic medicine   3: 424-32 (Journal)
Registered Authors
Hong, Sung-Kook
Keywords
Amniotic bands, ectopia cordis, limb anomalies, ventral midline defect
MeSH Terms
none
PubMed
26436108 Full text @ Mol Genet Genomic Med
Abstract
Limb body wall complex (LBWC) and amniotic band sequence (ABS) are multiple congenital anomaly conditions with craniofacial, limb, and ventral wall defects. LBWC and ABS are considered separate entities by some, and a continuum of severity of the same condition by others. The etiology of LBWC/ABS remains unknown and multiple hypotheses have been proposed. One individual with features of LBWC and his unaffected parents were whole exome sequenced and Sanger sequenced as confirmation of the mutation. Functional studies were conducted using morpholino knockdown studies followed by human mRNA rescue experiments. Using whole exome sequencing, a de novo heterozygous mutation was found in the gene IQCK: c.667C>G; p.Q223E and confirmed by Sanger sequencing in an individual with LBWC. Morpholino knockdown of iqck mRNA in the zebrafish showed ventral defects including failure of ventral fin to develop and cardiac edema. Human wild-type IQCK mRNA rescued the zebrafish phenotype, whereas human p.Q223E IQCK mRNA did not, but worsened the phenotype of the morpholino knockdown zebrafish. This study supports a genetic etiology for LBWC/ABS, or potentially a new syndrome.
Genes / Markers
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping