Table 2.

Phenotypes of initial Tet knockout mouse models.

Genotype	Phenotype	Reference
Tet1 null	Mice are viable, fertile, and grossly normal though some mutant mice have a slightly smaller body size at birth	Dawlaty et al., 2011
Tet1 null	Animals exhibited abnormal hippocampal long-term depression and impaired memory extinction	Rudenko et al., 2013; Zhang et al., 2013
Tet2 null	Approximately one-third of Tet2-/- and 8% of Tet2+/- mice died within 1 year of age because of the development of myeloid malignancies resembling characteristics of chronic myelomonocytic leukemia, myeloproliferative disorder-like leukemia, and myelodysplastic syndrome	Li et al., 2011
Tet3 null	Female mice depleted of Tet3 in the germ line show severely reduced fecundity and their heterozygous mutant offspring lacking maternal Tet3 suffer an increased incidence of developmental failure. Oocytes lacking Tet3 also seem to have a reduced ability to reprogram the injected nuclei from somatic cells	Gu et al., 2011
Tet1 and Tet2 null	Double deficient mice had reduced 5hmC and increase 5mC levels and abnormal methylation at various imprinted loci. Animals of both sexes were fertile with females having smaller ovaries and reduced fertility	Dawlaty et al., 2014