About   Help   FAQ
Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Hnrnpa3em1Ionsz
endonuclease-mediated mutation 1, Qiang Sun
MGI:5812384
Summary 1 genotype
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Hnrnpa3em1Ionsz/Hnrnpa3em1Ionsz C57BL/6J-Hnrnpa3em1Ionsz MGI:6472702


Genotype
MGI:6472702
hm1
Allelic
Composition
Hnrnpa3em1Ionsz/Hnrnpa3em1Ionsz
Genetic
Background
C57BL/6J-Hnrnpa3em1Ionsz
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hnrnpa3em1Ionsz mutation (0 available); any Hnrnpa3 mutation (22 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice die shortly after birth, probably due to neonatal hypoxia caused by lung developmental defects

respiratory system
• alveolar epithelium is thickened at P2
• lung size is significantly decreased at P2
• alveolar septum is disrupted at P2

nervous system
• the percentage of Dcx+CSFE+ cells among CFSE+ cells, representing neuronal progeny via direct neurogenic division, is decreased at E13.5
• mice show impaired neurogenesis of cortical neurons, in particular of early-born Ctip2+ deep layer neurons; the percentage of Ctip2+BrdUfull among BrdUfull cells is significantly decreased whereas the percentage of Cux1+BrdUfull or NeuN+BrdUfull among BrdUfull cells is relatively normal
• many PH3+ mitotic cells are abnormally stacked to form clusters at the ventricular zone (VZ) region at E14.5, unlike wild-type PH3+ cells which are aligned and attached to the apical surface of the VZ
• mice exhibit impaired neocortex development
• the layer thickness and numbers of Ctip2+ layer V cells, but not that of Cux1+ layer II-IV cells, are mildly but significantly reduced at P0
• the layer thickness and numbers of early formed Tbr1+ layer VI cells are significantly reduced at E18.5
• however, the number of Tbr2+ intermediate progenitor (IP) cells, which give rise to superficial layer neurons, is normal at E14.5
• mild but significant reduction in the thickness of the dorsal lateral cortex at P0

homeostasis/metabolism
• brain slices from E12.5 mice show an increase in caspase-9 signals that might be reflective of a DNA damage response
• brain slices show a significantly higher number of gammaH2AX+ cells at E13.5 as well as increased signals of phosphorylated-Atm (pS1981) in the VZ/SVZ regions at E14.5, suggesting activation of the DNA repair pathway
• neonatal hypoxia caused by lung developmental defects

cellular
• mice show a marked reduction in the percentage of mitotic neural progenitors (NPs) that enter a new round of the cell cycle (EdU+CFSE+ cells among CFSE+ cells), most likely due to mitotic delay
• the number of PH3+ mitotic cells is normal at E12.5 but markedly increased in the developing cortex at E14.5 and E17.5
• the percentage of ventricular zone (VZ) cells in prophase and pro-metaphase is significantly increased at E12.5, suggesting that the increase and abnormal distribution of mitotic cells might be due to cell cycle arrest
• although total number of proliferative radial glia cells (RGs) is normal at E14.5, the percentage of RGs at mitotic phase is increased, indicating a mitotic delay in RGs at the VZ
• live imaging of mitotic RGs in cultured E13.5 brain slices revealed a higher percentage of RGs with prolonged M-phase duration (>60 min/mitotic cell)
• analysis of the division angles of RGs at the VZ region demonstrated that neural progenitors (NPs) show an increase in oblique division (30-60 degrees) at the cost of near-vertical division (60-90 degrees) at E13.5
• prolonged mitosis of ventricular RGs causes a marked reduction in the production of deep layer neurons
• however, no differences in TUNEL or cleaved caspase-3 signals are noted at E12.5 or E14.5, indicating normal apoptosis
• the percentage of PH3+BrdU+cells among BrdU+ cells (i.e. cells arrested in mitosis) is significantly increased at E12.5
• at E13.5, many mitotic apical NPs exhibit chromatin bridges at anaphase as well as chromosome fragments derived from chromosome misalignment or mis-segregation of sister chromatids
• the percentage of Dcx+CSFE+ cells among CFSE+ cells, representing neuronal progeny via direct neurogenic division, is decreased at E13.5
• mice show impaired neurogenesis of cortical neurons, in particular of early-born Ctip2+ deep layer neurons; the percentage of Ctip2+BrdUfull among BrdUfull cells is significantly decreased whereas the percentage of Cux1+BrdUfull or NeuN+BrdUfull among BrdUfull cells is relatively normal
• brain slices from E12.5 mice show an increase in caspase-9 signals that might be reflective of a DNA damage response
• brain slices show a significantly higher number of gammaH2AX+ cells at E13.5 as well as increased signals of phosphorylated-Atm (pS1981) in the VZ/SVZ regions at E14.5, suggesting activation of the DNA repair pathway





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)
Citing These Resources
Funding Information
Warranty Disclaimer, Privacy Notice, Licensing, & Copyright
Send questions and comments to User Support.
last database update
10/29/2024
MGI 6.24
The Jackson Laboratory