Abstract
Autophagy is a catabolic process that takes place under both normal and adverse conditions and is important for the degradation of various organelles and proteins that are no longer needed. Thus, it can be viewed as both a constitutive recycling machinery and an adaptation mechanism. Increase in the activity of autophagy can be caused by multiple biotic and abiotic stress factors. Though intensive research in the past decade has elucidated many molecular details of plant autophagy, the mechanisms of induction and regulation of the process remain understudied. Here, we discuss the role of ATG8 proteins in autophagic signaling and regulation with an emphasis on the significance of ATG8 diversification for adapting autophagy to the changing needs of plants.
Highlights
Plants are unable to escape from unfavorable environmental conditions or damaging interactions with other organisms
The best studied example is the target of rapamycin (TOR) kinase which is a negative regulator of autophagy and its downregulation or inhibition leads to constitutive activation of autophagy (Liu and Bassham, 2010)
We focus on regulation of autophagy mainly through ATG8 diversification and specialization
Summary
Plants are unable to escape from unfavorable environmental conditions or damaging interactions with other organisms. In order to survive, they need to adapt to the changes in their surroundings as fast as possible Due to these characteristics, it is important for plants to efficiently acquire essential elements, produce and reuse metabolites, and optimize energy consumption by recycling of cellular components. One mechanism to degrade and recycle cytoplasmic material and provide building blocks in eukaryotic cells is autophagy (Li and Vierstra, 2012; Liu and Bassham, 2012; Avin-Wittenberg et al, 2018). Further studies with model organisms, including Arabidopsis thaliana, demonstrated high degree of conservation for the autophagic proteins in plants (Liu and Bassham, 2012). The best studied example is the target of rapamycin (TOR) kinase which is a negative regulator of autophagy and its downregulation or inhibition leads to constitutive activation of autophagy (Liu and Bassham, 2010). The TOR kinase transfers the Boycheva Woltering and Isono
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
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 callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
