**7. Conclusion**

Since the discovery of the ER stress- and osmotic stress-induced DCD/NRPmediated cell death response, considerable progress has been achieved toward deciphering the components and regulation of the pathway (**Figure 3**). We now know that the combination of multiple stresses synergistically activates a plant-specific PCD response that is initiated by induction of the stress-responsive transcription factor GmERD15, which, in turn, binds and activates the DCD/NRP promoter. Induction of the DCD/NRP genes *NRP-A* and *NRP-B* leads to the activation of a signal cascade that culminates with the upregulation of the transcription factors GmNAC81 and GmNAC30. The NAC transcription factors form a heterodimer to activate the expression of hydrolytic enzymes, including VPE, an executioner of vacuole-triggered programmed cell death. The stress-induced DCD/NRP-mediated cell death response is conserved in plants with similar regulatory mechanisms and represents a shared response to multiple stress signals. As a negative regulator of the stress-induced DCD/NRP-mediated cell death response, overexpression of the

**73**

*A Regulatory Circuit Integrating Stress-Induced with Natural Leaf Senescence*

ER-resident molecular chaperone BiP delays drought-induced senescence in tobacco and soybean plants and confers the increased adaptation of these transgenic lines under water deprivation conditions. This DCD/NNP-mediated stress-induced cell death program is also activated during age-dependent leaf senescence and contributes positively for the progression of the developmentally programmed senescence. Therefore, the plant-specific NRPs/NACs/VPE signaling module represents a regulatory circuit integrating stress-induced with natural leaf senescence.

We thank the Brazilian government agencies, Conselho Nacional de

Otto Teixeira Fraga1,2, Bruno Paes de Melo1,2, Luiz Fernando de Camargos1,2,

1 National Institute of Science and Technology in Plant-Pest Interactions, Bioagro,

2 Department of Biochemistry and Molecular Biology/BIOAGRO, Universidade

© 2019 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium,

Pedro Augusto Braga dos Reis1,2 and Elizabeth Pacheco Batista Fontes1,2\*

, Celio Cabral Oliveira1,2, Eduardo Bassi Simoni1,2,

Pessoal de Nível Superior (CAPES), for financial support.

The authors declare no conflict of interest.

Desenvolvimento Científico e Tecnológico (CNPq), Fundação de Amparo à Pesquisa do Estado de Minas Gerais (FAPEMIG), and Coordenação de Aperfeiçoamento de

*DOI: http://dx.doi.org/10.5772/intechopen.89498*

**Acknowledgements**

**Conflict of interest**

**Author details**

Debora Pellanda Fagundes1

Federal de Viçosa, Viçosa, Brazil

Universidade Federal de Viçosa, Viçosa, Brazil

\*Address all correspondence to: bbfontes@ufv.br

provided the original work is properly cited.

*A Regulatory Circuit Integrating Stress-Induced with Natural Leaf Senescence DOI: http://dx.doi.org/10.5772/intechopen.89498*

ER-resident molecular chaperone BiP delays drought-induced senescence in tobacco and soybean plants and confers the increased adaptation of these transgenic lines under water deprivation conditions. This DCD/NNP-mediated stress-induced cell death program is also activated during age-dependent leaf senescence and contributes positively for the progression of the developmentally programmed senescence. Therefore, the plant-specific NRPs/NACs/VPE signaling module represents a regulatory circuit integrating stress-induced with natural leaf senescence.
