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Autophagic Punctum

Multifaceted role of autophagy in regulating phosphate homeostasis and developmental root plasticity

ORCID Icon, , &
Article: 2247736 | Received 23 Jul 2023, Accepted 31 Jul 2023, Published online: 17 Aug 2023

Figures & data

Figure 1. Hypothetical models depicting multifaceted roles of autophagy in regulating the expression of PHT1 transporters and ATG8f/h-dependent lateral root formation. (A) Autophagy modulates the expression level of PHT1 transporters. Under Pi sufficiency, autophagy may positively regulate the translation of PHT1 transporters (i). Following Pi deficiency, an increased number of autophagosomes may contribute to the unconventional trafficking of de novo-synthesized PHT1 transporters en route to the plasma membrane, e.g., autophagy-dependent exocytosis (ii) or the trafficking of endocytosed PHT1 transporters back to the plasma membrane through the recycling endosomes (iii), which are otherwise sorted into the late endosomes for vacuolar degradation. (B) Pi starvation-induction of ATG8f and ATG8h is required to maintain the autophagic flux in the Pi-deplete root, which may mediate the lateral root development via hormone signaling-dependent or -independent selective autophagy.

Figure 1. Hypothetical models depicting multifaceted roles of autophagy in regulating the expression of PHT1 transporters and ATG8f/h-dependent lateral root formation. (A) Autophagy modulates the expression level of PHT1 transporters. Under Pi sufficiency, autophagy may positively regulate the translation of PHT1 transporters (i). Following Pi deficiency, an increased number of autophagosomes may contribute to the unconventional trafficking of de novo-synthesized PHT1 transporters en route to the plasma membrane, e.g., autophagy-dependent exocytosis (ii) or the trafficking of endocytosed PHT1 transporters back to the plasma membrane through the recycling endosomes (iii), which are otherwise sorted into the late endosomes for vacuolar degradation. (B) Pi starvation-induction of ATG8f and ATG8h is required to maintain the autophagic flux in the Pi-deplete root, which may mediate the lateral root development via hormone signaling-dependent or -independent selective autophagy.