DNA polymerase mu

DNA polymerase mu is a human protein encoded by the POLM is_associated_with::gene.

Function
Pol μ is a member of the X family of is_associated_with::DNA polymerases. It participates in resynthesis of damaged or missing nucleotides during the non-homologous end joining (NHEJ) pathway of is_associated_with::DNA repair. Pol μ interacts with Ku and DNA ligase IV, which also participate in NHEJ. It is structurally and functionally related to pol λ, and, like pol λ, pol μ has a is_associated_with::BRCT domain that is thought to mediate interactions with other DNA repair proteins. Unlike pol λ, however, pol μ has the unique ability to add a base to a blunt end that is templated by the overhang on the opposite end of the double-strand break. Pol μ is also closely related to terminal deoxynucleotidyl transferase (TdT), a specialized DNA polymerase that adds random nucleotides to DNA ends during is_associated_with::V(D)J recombination, the process by which B-cell and is_associated_with::T-cell receptor diversity is generated in the is_associated_with::vertebrate is_associated_with::immune system. Like TdT, pol μ participates in V(D)J recombination, but only during heavy chain rearrangements. This is distinct from pol λ, which is involved in light chain rearrangements.

POLM mutant mice
In polymerase mu mutant mice, hematopoietic cell development is defective in several peripheral and bone marrow cell populations with about a 40% decrease in bone marrow cell number that includes several hematopoietic lineages. Expansion potential of hematopoietic progenitor cells is also reduced. These characteristics correlate with reduced ability to repair double-strand breaks in hematopoietic tissue. Whole body gamma irradiation of polymerase mu mutant mice indicates that polymerase mu also has a role in double-strand break repair in other tissues unrelated to hematopoietic tissue. Thus polymerase mu has a significant role in maintaining genetic stability in hematopoietic and non-hematopoietic tissue.