Premium
Hi Tmtc4 Interacts with C3G, Wntless, and Zfhx4: A Yeast Two‐Hybrid Trap for Proteins Associated with Temtamy Syndrome
Author(s) -
Popli Tanav,
Lee Jiang,
Sherr Elliott
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.963.7
Subject(s) - biology , tetratricopeptide , agenesis of the corpus callosum , genetics , foxp2 , corpus callosum , population , wnt signaling pathway , gene , bioinformatics , microbiology and biotechnology , neuroscience , medicine , transcription factor , environmental health
Agenesis of the corpus callosum (ACC), a failure of the corpus callosum to develop, is linked to over 50 congenital syndromes. One syndrome which exhibits ACC as a symptom is Temtamy Syndrome, which also presents with craniofacial abnormalities, ocular colobomata, and mild mental retardation. Studies of some of these cases have provided possible candidate genes which may play a role in the etiology of the disorder. Transmembrane tetratricopeptide protein 4 (TMTC4) and Ankyrin repeat and MYND domain containing protein 1 (ANKMY1) were both identified as candidate genes through chromosomal analysis of individuals affected with Temtamy Syndrome. A yeast two‐hybrid protein trap was performed for both of these protein products, and interaction partners for each were identified. Fourteen protein‐coding sequences were identified as interaction partners for Tmtc4, and five protein‐coding sequences were identified as partners for Ankmy1. Only three of the proteins interacting with Tmtc4 were linked to embryonic brain development, and none of the five Ankmy1 interactors have known roles in brain development. The three interacting proteins found were Zfhx4, which regulates neural differentiation, Wntless, a member of the Wnt family and integral Wnt regulator, and C3G, a guanine exchange factor in the Ras pathway which regulates neural precursor population and neuron migration in the cerebral cortex. Future work should confirm these interactions in brain tissue, as well as investigate the effects of the aberrant forms of Tmtc4 on these interactions. These findings could provide much insight into the etiology of Temtamy Syndrome, and ultimately bring us closer to understanding the mechanisms of ACC.