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The plant WEE1 kinase is involved in checkpoint control activation in nematode‐induced galls
Author(s) -
Cabral Danila,
Banora Mohamed Youssef,
Antonino José Dijair,
Rodiuc Natalia,
Vieira Paulo,
Coelho Roberta R.,
Chevalier Christian,
Eekhout Thomas,
Engler Gilbert,
De Veylder Lieven,
GrossideSa Maria Fatima,
de Almeida Engler Janice
Publication year - 2020
Publication title -
new phytologist
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.742
H-Index - 244
eISSN - 1469-8137
pISSN - 0028-646X
DOI - 10.1111/nph.16185
Subject(s) - wee1 , nematode , biology , g2 m dna damage checkpoint , kinase , chek1 , botany , microbiology and biotechnology , cell cycle checkpoint , ecology , genetics , cell cycle , gene , cyclin dependent kinase 1
Summary Galls induced by plant‐parasitic nematodes involve a hyperactivation of the plant mitotic and endocycle machinery for their profit. Dedifferentiation of host root cells includes drastic cellular and molecular readjustments. In such a background, potential DNA damage in the genome of gall cells is evident. We investigated whether DNA damage checkpoint activation followed by DNA repair occurred, or was eventually circumvented, in nematode‐induced galls. Galls display transcriptional activation of the DNA damage checkpoint kinase WEE 1, correlated with its protein localization in the nuclei. The promoter of the stress marker gene SMR 7 was evaluated under the WEE 1‐knockout background. Drugs inducing DNA damage and a marker for DNA repair, PARP 1, were used to understand the mechanisms for coping with DNA damage in galls. Our functional study revealed that gall cells lacking WEE 1 conceivably entered mitosis prematurely, disturbing the cell cycle despite the loss of genome integrity. The disrupted nuclei phenotype in giant cells hinted at the accumulation of mitotic defects. In addition, WEE 1‐knockout in Arabidopsis and downregulation in tomato repressed infection and reproduction of root‐knot nematodes. Together with data on DNA ‐damaging drugs, we suggest a conserved function for WEE 1 in controlling G1/S cell cycle arrest in response to a replication defect in galls.