These mice carry an ENU-induced mutation and exhibit deafness with a loss of both ganglionic cells and the organ of corti.
The Jackson Laboratory cannot guarantee that cryorecovery of strains from the discontinued NIH-funded Neuroscience Mutagenesis Facility (NMF) will be successful or that the anticipated phenotype or genotype will be obtained. The cryorecovery fee for this effort will not be refunded or prorated if the recovery is unsuccessful or is in any way unsatisfactory. Genotyping will be the responsibility of the Purchaser.Read More +
These mutants were identified through head tilt, body leaning and circling behavior which can be detected at wean. ABR testing at 5-6 weeks of age showed these mutants also to be deaf at every frequency tested (click, 8, 16, 32kHz). Male or female mutants have been produced, and a colony can be maintained through normal breeding. Because of the phenotype and the map position of this mutation, a complementation test with Lhfpl5hscy (Stock No. 004640) has been performed; the results of two homozygote by heterozygote matings, i.e. 7 mutants in a total of 12 progeny, confirmed that nmf430 indeed represents an allele of Lhfpl5. Standard pathology work-up on one mutant (265 days of age) showed no abnormalities, however, serial sections of the ears revealed a loss of both ganglionic cells and the organ of corti (to view a section of control tissue, see Zheng et al., 2005).
This phenotypic deviant was generated by ethylnitrosourea (ENU) mutagenesis in C57BL/6J males (Stock No. 000664), in the Neuroscience Mutagenesis facility at The Jackson Laboratory. Mutagenized males were crossed to C57BL/6J females; G3 descendants of the mutagenized males were selected for neurological impairment.
|Allele Name||hurry-scurry 2 Jackson|
|Allele Type||Chemically induced (ENU)|
|Allele Synonym(s)||neuroscience mutagenesis facility, 430; NMF430; Tmhsnmf430|
|Gene Symbol and Name||Lhfpl5, lipoma HMGIC fusion partner-like 5|
|Strain of Origin||C57BL/6J|
|Molecular Note||This phenotypic mutation, identified in an ENU mutagenesis screen, was determined by complementation testing to be allelic with the original hurry-scurry mutation.|