Abstract

In plants, programmed cell death (PCD) has diverse, essential roles in vegetative and reproductive development, and in the responses to abiotic and biotic stresses. Despite the rapid progress in understanding the occurrence and functions of the diverse forms of PCD in plants, the signaling components and molecular mechanisms underlying the core PCD machinery remain a mystery. The roles of BAK1 (BRASSINOSTEROID INSENSITIVE 1-associated receptor kinase 1), an essential co-receptor of multiple receptor complexes, in the regulation of immunity and development- and defense-related PCD have been well characterized. However, the ways in which BAK1 functions in mediating PCD need to be further explored. In this review, different forms of PCD in both plants and mammals are discussed. Moreover, we mainly summarize recent advances in elucidating the functions and possible mechanisms of BAK1 in controlling diverse forms of PCD. We also highlight the involvement of post-translational modifications (PTMs) of multiple signaling component proteins in BAK1-mediated PCD.

Highlights

  • Plants have evolved surveillance systems and cellular responses to sustain their growth while protecting themselves against various environmental stresses, often through deploying programmed cell death (PCD) to balance the survival signaling with proper development patterns and abiotic stresses or microbial infections (Van Hautegem et al, 2015; Kabbage et al, 2017)

  • PCD was first reported in animals, where it serves as a mechanism to remove unwanted or damaged cells through development-related cell suicide and disease-related cell death (Zakeri et al, 1995; Raff, 1998)

  • It is believed that such an enhanced PCD phenotype in bak1 mutant upon pathogen infection is caused by the subsequent dysfunction of BRI1-associated receptor kinase 1 (BAK1)/BON1 suppressed cell death, which in turn activates the PEPR signaling pathway to reversely trigger cell death and to retain immunity to biotrophic pathogens (Yamada et al, 2016)

Read more

Summary

Introduction

Plants have evolved surveillance systems and cellular responses to sustain their growth while protecting themselves against various environmental stresses, often through deploying programmed cell death (PCD) to balance the survival signaling with proper development patterns and abiotic stresses or microbial infections (Van Hautegem et al, 2015; Kabbage et al, 2017). It is believed that such an enhanced PCD phenotype in bak1 mutant upon pathogen infection is caused by the subsequent dysfunction of BAK1/BON1 suppressed cell death, which in turn activates the PEPR signaling pathway to reversely trigger cell death and to retain immunity to biotrophic pathogens (Yamada et al, 2016).

Results
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call