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The protocadherin 11X/Y ( PCDH11X/Y ) gene pair as determinant of cerebral asymmetry in modern Homo sapiens
Author(s) -
Priddle Thomas H.,
Crow Timothy J.
Publication year - 2013
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/nyas.12042
Subject(s) - protocadherin , homo sapiens , subplate , biology , homology (biology) , genetics , locus (genetics) , gene , human brain , brain asymmetry , corpus callosum , asymmetry , cerebral cortex , neuroscience , lateralization of brain function , cadherin , physics , quantum mechanics , sociology , anthropology , cell
Annett's right‐shift theory proposes that human cerebral dominance (the functional and anatomical asymmetry or torque along the antero‐posterior axis) and handedness are determined by a single “right‐shift” gene. Familial transmission of handedness and specific deviations of cerebral dominance in sex chromosome aneuploidies implicate a locus within an X–Y homologous region of the sex chromosomes. The Xq21.3/Yp11.2 human‐specific region of homology includes the protocadherin 11X/Y ( PCDH11X/Y ) gene pair, which encode cell adhesion molecules subject to accelerated evolution following the separation of the human and chimpanzee lineages six million years ago. PCDH11X and PCDH11Y , differentially regulated by retinoic acid, are highly expressed in the ventricular zone, subplate, and cortical plate of the developing cerebral cortex. Both proteins interact with β‐catenin, a protein that plays a role in determining axis formation and regulating cortical size. In this way, the PCDH11X/Y gene pair determines cerebral asymmetry by initiating the right shift in Homo sapiens .