A regulatory module controlling stress-induced cell cycle arrest in Arabidopsis

Takahashi, Nobutaka; Ogita, Nobuo; Takahashi, Tomonobu; Taniguchi, Shoji; Tanaka, Maho; Seki, Motoaki; Umeda, Masaaki

doi:10.7554/elife.43944

Cited by 100 publications

(130 citation statements)

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“…The down-regulation of CDKB2;1 in response to DNA damage could thus result from the concomitant degradation of the protein by the APC/C and repression of the CDKB2;1 gene by Rep-MYB3Rs. Very recently, the ANAC044 and ANAC085 transcription factors, the two SOG1 closest relatives that are also SOG1 targets (Ogita et al, 2018), were reported to promote rep-MYB3R accumulation in response to DNA damage (Takahashi et al, 2019). Genetic analysis showed that ANAC044 and ANAC085 function in the same pathway as SOG1 to control cell cycle arrest through rep-MYB3R accumulation but not activation of SMR genes or DNA repair genes.…”

Section: Main Players In Ddr Signalingmentioning

confidence: 99%

“…Genetic analysis showed that ANAC044 and ANAC085 function in the same pathway as SOG1 to control cell cycle arrest through rep-MYB3R accumulation but not activation of SMR genes or DNA repair genes. To date, it remains unclear how ANAC044 and ANAC085 modulate Rep-MYB3R protein levels, as they do not directly target Rep-MYB genes, but this pathway could involve the regulation of proteins involved in the degradation of Rep-MYBs such as F-box proteins (Takahashi et al, 2019). Figure 2 summarizes how DDR triggers cell cycle arrest either in S phase or in G2 phase, and can lead to cell differentiation and endoreduplication.…”

Section: Main Players In Ddr Signalingmentioning

confidence: 99%

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The Plant DNA Damage Response: Signaling Pathways Leading to Growth Inhibition and Putative Role in Response to Stress Conditions

et al. 2019

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Maintenance of genome integrity is a key issue for all living organisms. Cells are constantly exposed to DNA damage due to replication or transcription, cellular metabolic activities leading to the production of Reactive Oxygen Species (ROS) or even exposure to DNA damaging agents such as UV light. However, genomes remain extremely stable, thanks to the permanent repair of DNA lesions. One key mechanism contributing to genome stability is the DNA Damage Response (DDR) that activates DNA repair pathways, and in the case of proliferating cells, stops cell division until DNA repair is complete. The signaling mechanisms of the DDR are quite well conserved between organisms including in plants where they have been investigated into detail over the past 20 years. In this review we summarize the acquired knowledge and recent advances regarding the DDR control of cell cycle progression. Studying the plant DDR is particularly interesting because of their mode of development and lifestyle. Indeed, plants develop largely post-embryonically, and form new organs through the activity of meristems in which cells retain the ability to proliferate. In addition, they are sessile organisms that are permanently exposed to adverse conditions that could potentially induce DNA damage in all cell types including meristems. In the second part of the review we discuss the recent findings connecting the plant DDR to responses to biotic and abiotic stresses.

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Section: Main Players In Ddr Signalingmentioning

confidence: 99%

Section: Main Players In Ddr Signalingmentioning

confidence: 99%

The Plant DNA Damage Response: Signaling Pathways Leading to Growth Inhibition and Putative Role in Response to Stress Conditions

et al. 2019

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“…The SOG1 direct targets include genes implicated in response to abiotic stresses and pathogen infection ( Ogita et al., 2018 ). Two of SOG1 targets, ANAC044 and ANAC085 , are its closest relatives in the NAC TF family and were suggested to also participate in SOG1-mediated induction of stem cell death ( Takahashi et al., 2019 ). However, it is not clear which key downstream PCD effectors are controlled by SOG1/ANAC008 signaling.…”

Section: Nac Transcription Factorsmentioning

confidence: 99%

Stressed to Death: The Role of Transcription Factors in Plant Programmed Cell Death Induced by Abiotic and Biotic Stimuli

et al. 2020

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Programmed cell death (PCD) is a genetically controlled pathway that plants can use to selectively eliminate redundant or damaged cells. In addition to its fundamental role in plant development, PCD can often be activated as an essential defense response when dealing with biotic and abiotic stresses. For example, localized, tightly controlled PCD can promote plant survival by restricting pathogen growth, driving the development of morphological traits for stress tolerance such as aerenchyma, or triggering systemic pro-survival responses. Relatively little is known about the molecular control of this essential process in plants, especially in comparison to well-described cell death models in animals. However, the networks orchestrating transcriptional regulation of plant PCD are emerging. Transcription factors (TFs) regulate the clusters of stimuli inducible genes and play a fundamental role in plant responses, such as PCD, to abiotic and biotic stresses. Here, we discuss the roles of different classes of transcription factors, including members of NAC, ERF and WRKY families, in cell fate regulation in response to environmental stresses. The role of TFs in stress-induced mitochondrial retrograde signaling is also reviewed in the context of life-and-death decisions of the plant cell and future research directions for further elucidation of TF-mediated control of stress-induced PCD events are proposed. An increased understanding of these complex signaling networks will inform and facilitate future breeding strategies to increase crop tolerance to disease and/or abiotic stresses.

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“…Recently, two independent studies have demonstrated that SOG1 regulates the expression of almost all the genes that are induced when DNA is damaged, including other transcription factors from the same family (Bourbousse et al, 2018; Ogita et al, 2018). Now, in eLife, Masaaki Umeda and colleagues from the Nara Institute of Science and Technology, the RIKEN Center for Sustainable Resource Science and the RIKEN Cluster for Pioneering Research – with Naoki Takahashi as first author – report on the roles of two of these SOG1-like transcription factors, ANAC044 and ANAC085 (Takahashi et al, 2019).…”

mentioning

confidence: 99%

“…If stabilized, these proteins maintain the cells in the phase just before division (G2/M arrest) by binding to and repressing the genes essential for cell division to proceed. It is still unclear how Rep-MYBs are stabilized, or how SOG1 and ANAC044/ANAC085 may trigger cell death (Takahashi et al, 2019).…”

mentioning

confidence: 99%