• oxygen
• hypoxia
• meristem
• development
• stm

Scarcity of oxygen in plant tissues has been traditionally identified as a result of exogenous stress
such as flooding. Recently however, the existence of endogenous hypoxia enclosing meristematic tissues was
shown via direct measurement of oxygen levels and the employment of genetically encoded oxygen-signaling
biosensors. The existence of hypoxic domains encompassing these meristematic regions was shown to act as
a signaling cue to direct organogenesis and vernalization by preventing the O2-dependent proteolysis of
certain transcriptional regulators in meristems. The ability of plants to sense oxygen levels largely relies on
the activity of PLANT CYSTEINE OXIDASES (PCO), which use molecular oxygen as a cofactor to label target
proteins for proteasomal degradation via the N-degron pathway. In this manner, PCOs were shown to be
essential to regulate the response to acute hypoxia; however, the specific developmental pathways affected
by low oxygen signaling still need to be identified.
By analyzing the transcriptome of the knock-out mutant for four of the five Arabidopsis PCOs we
detected differential expression of several genes directly involved in plant development; this altered
transcriptomic pattern correlated with severely altered plastochron and delayed leaf differentiation. Further
analysis showed that the stabilization of direct targets of PCO was sufficient to induce ectopic expression of
SHOOT-MERISTEMLESS (STM) in Arabidopsis thaliana leaves. This led us to the hypothesis that oxygenmediated degradation of ERFVII transcription factors may play a role to prevent the expression of meristem
cell fate genes outside of their canonical meristematic domains, while hypoxia-dependent stabilization of
ERFVII may contribute to the maintenance of their expression in the shoot apical meristem.