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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Kif3atm1Noh
targeted mutation 1, Nobutaka Hirokawa
MGI:2181727
Summary 1 genotype
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Kif3atm1Noh/Kif3atm1Noh involves: 129S4/SvJae * C57BL/6J MGI:3512508


Genotype
MGI:3512508
hm1
Allelic
Composition
Kif3atm1Noh/Kif3atm1Noh
Genetic
Background
involves: 129S4/SvJae * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Kif3atm1Noh mutation (0 available); any Kif3a mutation (33 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Severe developmental abnormalities in Kif3atm1Noh/Kif3atm1Noh mice

mortality/aging
• homozygotes die at midgestation before 10.5 dpc, possibly due to cardiac insufficiency

cardiovascular system
• at 9.5 dpc, homozygotes display a hypoplastic, underdeveloped myocardium
• ~20% of homozygotes show incomplete cardiac looping (tuba rectae)
• ~40% of homozygous embryos show cardiac L-loops (situs inversus); in contrast, almost all wild-type embryos display a D-loop heart (situs solitas)
• at 9.5 dpc, homozygotes display severe distention of the pericardium
• at E9.5 dpc, extensive pericardial effusion leads to circulatory insufficiency

embryo
• mutant show near absence of mature monocilia on nodal pit cells
• either no or extremely short cilia are observed
• homozygotes show patterning defects in the neural tube, heart, brachial arches, and lower truncal mesoderm, resulting in severely underdeveloped posterior structures
• at 9.5 dpc, embryonic turning remains incomplete in most cases, suggesting growth retardation
• homozygotes display mesodermal and caudal dysgenesis
• wild-type embryos contain motile monocilia on nodal pit cells and generate a leftward flow of extraembryonic fluid (nodal flow); in contrast, mutants lack motile monocilia and generate no nodal flow, suggesting impaired L-R determination
• at 9.5 dpc, mutant embryos are smaller than wild-type embryos
• at 9.5 dpc, mutant embryos exhibit swelling and degeneration of the neural tube
• at this stage, thinning of the neural tube wall is observed
• at 9.5 dpc, staggering of the neural tube is noted at the incomplete turning region
• at 9.5 dpc, homozygotes exhibit degeneration in the lower truncal part and abnormal somitegenesis (sirenomelia); somites appear highly disorganized

growth/size/body
• at 9.5 dpc, mutant embryos are smaller than wild-type embryos

nervous system
• at 9.5 dpc, mutant embryos exhibit swelling and degeneration of the neural tube
• at this stage, thinning of the neural tube wall is observed
• at 9.5 dpc, staggering of the neural tube is noted at the incomplete turning region
• at 9.5 dpc, the neural tube dysmorphology resembles hydrocephalus

homeostasis/metabolism
• at E9.5 dpc, extensive pericardial effusion leads to circulatory insufficiency

cellular
• mutant show near absence of mature monocilia on nodal pit cells
• either no or extremely short cilia are observed

muscle
• at 9.5 dpc, homozygotes display a hypoplastic, underdeveloped myocardium





Contributing Projects:
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO)
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last database update
10/22/2024
MGI 6.24
The Jackson Laboratory