| Literature DB >> 31505035 |
Danila Cabral1, Mohamed Youssef Banora2,3, José Dijair Antonino1,4,5, Natalia Rodiuc1,4, Paulo Vieira1, Roberta R Coelho1,4, Christian Chevalier6, Thomas Eekhout7,8, Gilbert Engler1, Lieven De Veylder7,8, Maria Fatima Grossi-de-Sa4, Janice de Almeida Engler1.
Abstract
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 WEE1, correlated with its protein localization in the nuclei. The promoter of the stress marker gene SMR7 was evaluated under the WEE1-knockout background. Drugs inducing DNA damage and a marker for DNA repair, PARP1, were used to understand the mechanisms for coping with DNA damage in galls. Our functional study revealed that gall cells lacking WEE1 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, WEE1-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 WEE1 in controlling G1/S cell cycle arrest in response to a replication defect in galls.Entities:
Keywords: zzm321990Arabidopsis thalianazzm321990; zzm321990Solanum lycopersicumzzm321990; WEE1 kinase; cell cycle; checkpoint control; galls; root-knot nematode
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Year: 2019 PMID: 31505035 DOI: 10.1111/nph.16185
Source DB: PubMed Journal: New Phytol ISSN: 0028-646X Impact factor: 10.151