In a groundbreaking study published in Cell on May 22, researchers from the Institute of Genetics and Developmental Biology (IGDB) of the Chinese Academy of Sciences have made a significant discovery in the field of plant regeneration. Led by Prof. Li Chuanyou, the team has identified REGENERATION FACTOR1 (REF1) as the primary local wound signal that triggers plant regenerative responses.
Plants, unlike animals, frequently experience injuries and have developed remarkable abilities to deal with them. When plants are wounded, they activate defense mechanisms to prevent infections and simultaneously initiate cellular reprogramming to repair damaged tissues and regenerate lost body parts.
While the signaling pathways for wound-induced defense responses in plants are well-known, the molecular mechanisms governing regenerative responses have long been elusive. The identification of REF1 as a key player in plant regeneration opens up new possibilities for enhancing the regeneration capacity of crops, especially those that are challenging to transform.
The variation in regenerative capacity among plant species and genotypes has been a significant obstacle in leveraging genetic transformation and genome editing technologies for crop improvement. The discovery of REF1 as a primary wound signal sheds light on the complex interplay between regeneration and defense mechanisms in plants.
The researchers observed that a mutant, spr9, exhibited defects in both wound-induced defense responses and regenerative capabilities. This mutant highlighted the dual role of the SPR9 gene in regulating local defense and organ regeneration processes.
This study not only addresses a long-standing question in plant biology regarding organ regeneration but also paves the way for future research aimed at enhancing crop regeneration efficiency through targeted genetic modifications. The findings offer valuable insights into the intricate mechanisms underlying plant wound responses and open up new avenues for improving crop resilience and productivity.