Exploring the linguistic complexity of third-grade numerical literacy.

Reading numbers aloud, a central aspect of numerical literacy, is a challenging skill to acquire, but the origins of this difficulty remain poorly understood. To investigate this matter, we examined the performance of 127 third- and fourth-grade children who read aloud, in Hebrew, numbers with 2-5 digits. We found several key observations. First, we observed a substantial variation among the 3rd graders-7% and 59% errors in the top and bottom deciles, respectively. Second, the task difficulty stemmed from syntactic processing: Most errors were distortions of the number's syntax, as opposed to digit substitutions or transpositions, and the main factor affecting a specific number's difficulty was not its magnitude, as is commonly assumed, but rather its syntactic structure. Third, number reading performance was not predicted by a school-like task that assessed syntactic-conceptual knowledge of the decimal system structure, but rather by knowledge of specific syntactic-verbal rules, suggesting that the syntactic-verbal knowledge is separate from the syntactic-conceptual knowledge. Last, there was a double dissociation between 4-digit numbers and 5-digit numbers, which in Hebrew have completely different syntactic structures: Half of the children showed a significant advantage in one number length compared to the other, with equal numbers of children preferring either length. This indicates that the different syntactic-verbal rules are learned relatively independently of each other, with little or no generalization from one rule to another. In light of these findings, we propose that schools should specifically teach number reading, with focus on specific syntactic-verbal rules.

A Myo6 mutation destroys coordination between the myosin heads, revealing new functions of myosin VI in the stereocilia of mammalian inner ear hair cells.

Myosin VI, found in organisms from Caenorhabditis elegans to humans, is essential for auditory and vestibular function in mammals, since genetic mutations lead to hearing impairment and vestibular dysfunction in both humans and mice. Here, we show that a missense mutation in this molecular motor in an ENU-generated mouse model, Tailchaser, disrupts myosin VI function. Structural changes in the Tailchaser hair bundles include mislocalization of the kinocilia and branching of stereocilia. Transfection of GFP-labeled myosin VI into epithelial cells and delivery of endocytic vesicles to the early endosome revealed that the mutant phenotype displays disrupted motor function. The actin-activated ATPase rates measured for the D179Y mutation are decreased, and indicate loss of coordination of the myosin VI heads or 'gating' in the dimer form. Proper coordination is required for walking processively along, or anchoring to, actin filaments, and is apparently destroyed by the proximity of the mutation to the nucleotide-binding pocket. This loss of myosin VI function may not allow myosin VI to transport its cargoes appropriately at the base and within the stereocilia, or to anchor the membrane of stereocilia to actin filaments via its cargos, both of which lead to structural changes in the stereocilia of myosin VI-impaired hair cells, and ultimately leading to deafness.