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Selective chromatid segregation mechanism invoked for the human congenital mirror hand movement disorder development by RAD51 mutations: A Hypothesis

Monday, September 22, 2014 — Poster Session II

4:00 p.m. – 6:00 p.m.

FAES Academic Center




  • Amar Klar


The vertebrate body plan externally is largely symmetrical across the midline but internal organs develop asymmetrically. The biological basis of asymmetric organ development has been investigated extensively for years, although the proposed mechanisms remain controversial. By comparison, the biological origin of external organs symmetry has not been extensively investigated. Bimanual hand control is one such external organs symmetry allowing independent motor control movements of both hands to a person. This gap in our knowledge is illustrated by the recent reports of heterozygous rad51 mutations causing mysterious symptoms of congenital mirror hand movement disorder (MM) in humans with 50% penetrance by an unknown mechanism. The analysis of mutations that vary symmetry or asymmetry could be exploited to decipher the mechanisms of laterality development. Here I present a hypothesis for explaining 50% penetrance of the rad51 mutation. The MM’s origin is explained with the Somatic Strand-specific Imprinting and selective sister chromatid Segregation (SSIS) hypothesis proposed originally as the mechanism of asymmetric cell division to promote visceral organs body plan laterality development in vertebrates. By hypothesis, random sister chromatid segregation in mitosis occurs of a specific chromosome due to rad51/RAD51 constitution causing MM disorder in 50% of subjects.

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