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Area of Science:

  • Plant Biology
  • Epigenetics
  • Molecular Signaling

Background:

  • Nutrients and energy are crucial for plant development.
  • The Target of Rapamycin (TOR) kinase integrates nutrient signals to control growth.
  • TOR's role in developmental transitions and differentiation is not fully understood.

Purpose of the Study:

  • To investigate how glucose-activated TOR kinase influences epigenetic modifications and developmental programs in Arabidopsis thaliana.
  • To identify and characterize TOR targets involved in regulating cell fate and development.

Main Methods:

  • Genome-wide analysis of histone H3 trimethylation at K27 (H3K27me3).
  • Identification of FERTILIZATION-INDEPENDENT ENDOSPERM (FIE) as a TOR target.
  • Phosphorylation site mutation analysis of FIE.
  • Transcriptome reprogramming analysis.
  • Investigation of the glucose-TOR-FIE-Polycomb repressive complex 2 (PRC2) signaling pathway.

Main Results:

  • Glucose-activated TOR kinase controls genome-wide H3K27me3 levels in Arabidopsis.
  • FERTILIZATION-INDEPENDENT ENDOSPERM (FIE) is a direct TOR target, and its phosphorylation by TOR drives nuclear translocation.
  • Disruption of FIE phosphorylation abrogates H3K27me3, alters the transcriptome, and impairs organogenesis.
  • The glucose-TOR-FIE-PRC2 pathway regulates the vernalization-induced floral transition.

Conclusions:

  • The glucose-TOR-FIE-PRC2 signaling axis acts as a nutritional checkpoint.
  • This pathway epigenetically silences genes controlling stem cell fate and organ patterning.
  • Nutrient signaling directly reprograms the epigenome, influencing developmental transitions in plants.