Correction: An SR protein is essential for activating DNA repair in malaria parasites

Manish Goyal; Brajesh Kumar Singh; Karina Simantov; Yotam Kaufman; Shiri Eshar; Ron Dzikowski

doi:10.1242/jcs.259460

Correction: An SR protein is essential for activating DNA repair in malaria parasites

Journal of Cell Science ◽

10.1242/jcs.259460 ◽

2021 ◽

Vol 134 (21) ◽

Author(s):

Manish Goyal ◽

Brajesh Kumar Singh ◽

Karina Simantov ◽

Yotam Kaufman ◽

Shiri Eshar ◽

...

Keyword(s):

Dna Repair ◽

Malaria Parasites ◽

Sr Protein

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An SR protein is essential for activating DNA repair in malaria parasites

Journal of Cell Science ◽

10.1242/jcs.258572 ◽

2021 ◽

Author(s):

Manish Goyal ◽

Brajesh Kumar Singh ◽

Karina Simantov ◽

Yotam Kaufman ◽

Shiri Eshar ◽

...

Keyword(s):

Dna Damage ◽

Dna Repair ◽

Rna Splicing ◽

Dna Double Strand Breaks ◽

Malaria Parasites ◽

Sr Protein ◽

Strand Breaks ◽

Dna Damaging Agents ◽

Parasite Viability ◽

Harsh Conditions

Plasmodium falciparum, the parasite responsible for the deadliest form of human malaria, replicates within the erythrocytes of its host where it encounters numerous pressures that cause extensive DNA damage, which must be repaired efficiently to ensure parasite survival. Malaria parasites, which lost the NHEJ pathway for repairing DNA double strand breaks, have evolved unique mechanisms that enable them to robustly maintain genome integrity under such harsh conditions. However, the nature of these adaptations is unknown. We show that a highly conserved RNA splicing factor, PfSR1, plays an unexpected and crucial role in DNA repair in malaria parasites. Using an inducible and reversible system to manipulate PfSR1 expression, we demonstrate that this protein is recruited to foci of DNA damage. While loss of PfSR1 does not impair parasite viability, the protein is essential for parasites recovery from DNA damaging agents or exposure to artemisinin, the first line antimalarial drug, demonstrating its necessity for DNA repair. These findings provide key insights into the evolution of DNA repair pathways in malaria parasites as well as the parasite's ability to recover from antimalarial treatment.

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