Phenotypes associated with this allele

• Allele Symbol: Anapc2^tm2Kna
• Allele Name: targeted mutation 2, Kim Nasmyth
• Allele ID: MGI:3029826
• Summary: 2 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Anapc2^tm2Kna/Anapc2^tm2Kna	involves: 129P2/OlaHsd * C57BL/6	MGI:3686617
cn2	Anapc2^tm1Kna/Anapc2^tm2Kna Tg(Mx1-cre)1Cgn/0	involves: 129P2/OlaHsd * C57BL/6 * CBA	MGI:3686618

Genotype
MGI:3686617

hm1

• Allelic Composition: Anapc2^tm2Kna/Anapc2^tm2Kna
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6

• ♀: phenotype observed in females
• ♂: phenotype observed in males
• N: normal phenotype

mortality/aging

embryonic lethality between implantation and somite formation, complete penetrance ( J:87782 )

• die before E6.5 as no homozygous embryos are found at E6.5 or E9.5

Genotype
MGI:3686618

cn2

• Allelic Composition: Anapc2^tm1Kna/Anapc2^tm2Kna; Tg(Mx1-cre)1Cgn/0
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6 * CBA

mortality/aging

premature death ( J:87782 )

• most die during the second week after the first pI/C injection to induce cre-mediated deletion of Anapc2 in the liver and lymphocytes

liver/biliary system

decreased liver glycogen level ( J:87782 )

• hepatocytes of mutants treated with pI/C lack glycogen

abnormal hepatocyte morphology ( J:87782 )

• hepatocytes are greatly enlarged, lack nuclear membranes, and contain condensed chromosomes in 6 of 10 mutants after pI/C injection

• 72% of mitotic hepatocytes are in a prometaphase-like state with condensed chromatin

abnormal liver physiology ( J:87782 )

• levels of the liver enzymes alanine aminotransferase and glutamate dehydrogenase are highly elevated in pI/C injected mutants, indicating functional impairment and damage of hepatocytes

increased hepatocyte proliferation ( J:87782 )

• quiescent hepatocytes of some but not all livers enter into a proliferative state, resulting in a mitotic arrest

• 2/3 hepatectomy in mutants transplanted with wild-type bone marrow and treated with pI/C caused 70% of hepatoctyes to re-enter the cell cycle and embark on proliferation and arrest in metaphase 3 to 5 days after hepatectomy

liver failure ( J:87782 )

• die from acute liver failure after pI/C injection

hematopoietic system

anemia ( J:87782 )

• the 4 of 10 mutants injected with pI/C with normal livers and 2 of 6 with abnormal livers show severe anemia

decreased hemoglobin content ( J:87782 )

• the 4 of 10 mutants injected with pI/C with normal livers show decreased hemoglobin levels

homeostasis/metabolism

increased circulating bilirubin level ( J:87782 )

• levels of bilirubin are highly elevated in pI/C injected mutants

abnormal enzyme/coenzyme level ( J:87782 )

• levels of the liver enzymes alanine aminotransferase and glutamate dehydrogenase are highly elevated in pI/C injected mutants, indicating functional impairment and damage of hepatocytes

decreased liver glycogen level ( J:87782 )

• hepatocytes of mutants treated with pI/C lack glycogen

skeleton

abnormal bone marrow morphology ( J:87782 )

• develop severe bone marrow aplasia within 4 days of pI/C injection; by day 4, majority of nucleated cells disappear from the bone marrow which contains mainly erythrocytes and a few lymphocytes

cellular

increased hepatocyte proliferation ( J:87782 )

• quiescent hepatocytes of some but not all livers enter into a proliferative state, resulting in a mitotic arrest

• 2/3 hepatectomy in mutants transplanted with wild-type bone marrow and treated with pI/C caused 70% of hepatoctyes to re-enter the cell cycle and embark on proliferation and arrest in metaphase 3 to 5 days after hepatectomy