Plasmodium falciparum DNA repair dynamics reveal unique roles for TLS polymerases and PfRad51 in genome diversification.

ABSTRACT: The human malaria parasite, Plasmodium falciparum, faces unique DNA repair challenges; it is haploid, undergoes asynchronous mitosis termed schizogony, and lacks canonical non-homologous end joining (C-NHEJ). Yet, it has adapted DNA repair pathways that enable survival in distinct environments, including human erythrocytes and hepatocytes, as well as the mosquito vector. Plasmodium falciparum chromosomes are partitioned into a conserved core genome and highly diverse subtelomeric regions containing hypervariable, multicopy gene families, including var, which encodes a critical parasite virulence factor. The molecular mechanisms maintaining this chromosomal structure remain unclear. Here, we describe specific DNA repair pathways that distinguish hypervariable subtelomeric regions from the c

SUBMITTER: Vishwanatha A 

PROVIDER: S-EPMC12641262 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature