The recessive mutant mice bate palmas (bapa) - claps in Portuguese arose from 
N-ethyl-N-nitrosourea mutagenesis. A single nucleotide, T > C, change in exon 
13, leading to a Thr1289 Ala substitution, was identified in the lysine 
(K)-specific methyltransferase 2D gene (Kmt2d) located on chromosome 15. 
Mutations with a loss-of-function in the KMT2D gene on chromosome 12 in humans 
are responsible for Kabuki syndrome (KS). Phenotypic characterization of the 
bapa mutant was performed using a behavioral test battery to evaluate the 
parameters related to general activity, the sensory nervous system, the 
psychomotor system, and the autonomous nervous system, as well as to measure 
motor function and spatial memory. Relative to BALB/cJ mice, the bapa mutant 
showed sensory and psychomotor impairments, such as hypotonia denoted by a 
surface righting reflex impairment and hindquarter fall, and a reduction in the 
auricular reflex, suggesting hearing impairment. Additionally, the enhanced 
general activity showed by the increased rearing and grooming frequency, 
distance traveled and average speed possibly presupposes the presence of 
hyperactivity of bapa mice compared with the control group. A slight motor 
coordination dysfunction was showed in bapa mice, which had a longer crossing 
time on the balance beam compared with BALB/cJ controls. Male bapa mice also 
showed spatial gait pattern changes, such as a shorter stride length and shorter 
step length. In conclusion, the bapa mouse may be a valuable animal model to 
study the mechanisms involved in psychomotor and behavior impairments, such as 
hypotonia, fine motor coordination and hyperactivity linked to the Kmt2d 
mutation.