Table 1.

Asxl1 knockout and mutant Asxl1 expressing mice studies

Mice	Peripheral blood phenotypes	HSC/HSPC phenotypes	Myeloid malignancies	Histone modifications	Gene expressions	References
Asxl1tm1Bc mutant mice	Decreased matured B-cell	Decreased formation of myeloid/erythroid colonies	Asxl1tm1Bc mutant mice did not develop AML up to 58 weeks	Not described	Not described	[97]
Mx1-Cre/Vav-Cre conditional Asxl1 knockout mice	Leukocytopenia and anemia in old (> 6 months) mouse	Increase in LT-HSCs and LSK fractions	Development of Progressive MDS-like disease	Reduced global level of H3K27me3	Increased expression of Hoxa7/9	[25]
Constitutive Asxl1 knockout mice	Leukocytopenia, anemia, thrombocytopenia	Decrease in LSK fractions, increase in GMP fractions	Asxl1+/− mice developed mild MDS-like disease	Reduced global level of H3K27me3/H3K4me3	Increased expression of Hoxa5/7/9/10	[26]
Retroviral mutant ASXL1 expression in mouse BMT	Leukocytopenia, anemia, thrombocytopenia	Not described	MDS-like disease after a long latency (> 1 year)	Reduced global level of H3K27me3	Increased expression of miR125a and Hoxa9	[28]
Asxl1 Y588X mutant expressing transgenic mice	Anemia	Increase in ST-HSCs and LSK fractions	A part of mice developed myeloid malignancies	Increased level of H3K122ac at Prdm16 promoter locus	Increased expression of Prdm16	[33]
Vav-Cre Rosa26 mutant Asxl1 knockin mice	Decreased in RBC count	Decrease in LT-HSCs and LSK fractions	Knockin mice alone did not develop MDS/AML but promoted MDS/AML development with RUNX1 mutant	Reduced global level of H2AK119ub/H3K4me3, reduced level of H3K27me3 at Hoxa loci	Decreased expression of Id3, Runx1, Sox6 and Tjp1	[29]
Constitutive locus Asxl1 G643Wfs mutant knockin mice	Leukocytosis and increase in RBC count in aged (18 months) male mice	Competitive serial transplantation assay showed disadvantage	Knockin mice alone did not develop myeloid malignancies within 18 months	Change in distribution of H3K27me3 peak	Not described	[115]
Constitutive locus Asxl1 G643Wfs mutant knockin mice	Leukocytopenia/thrombocytosis in aged (12 months) mouse	Decrease in LT-HSCs and LSK fractions	A part of mice developed MDS/MPN disease in long latency (18–24 months)	Reduced level of H2AK119ub at p16Ink4a locus	Increased expression of Hoxa7/9/10 and p16Ink4a	[116]