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De Angelis, M.

Publications and source records attributed to De Angelis, M..

2 recordsLinked to original sources

Arabidopsis lateral shoots display two distinct phases of growth angle control

Shoot growth angle is a fundamental determinant of plant form. In their later development, lateral branches maintain gravitropic setpoint angles (GSAs) in which growth is set and maintained relative to gravity. The typically non-vertical GSAs are the product of an auxin-dependent antigravitropic offset that counteracts underlying gravitropic response in the branch (Roychoudhry et al., 2013). Here we describe an earlier phase of branch development in which the young lateral shoot grows rootward, independently of gravity, promoting a spreading growth habit. In normal development, this phase of growth is terminated with the onset of the GSA programme, with branches then growing upwards to assume their mature form. The biophysical basis of the early rootward phase of branch growth can be traced back to greater cell proliferation on the upper, adaxial side that upon expansion, drives asymmetric growth. Our data indicate that cytokinin is involved in this process and that the transcription factor TCP1 is an important regulator of lateral shoot adaxial identity and differential ad-abaxial cell proliferation.

plant biology↗

Mediobasal hypothalamic FKBP51 acts as a molecular switch linking autophagy to whole-body metabolism

The mediobasal hypothalamus (MBH) is the central region in the physiological response to metabolic stress. The FK506-binding protein 51 (FKBP51) is a major modulator of the stress response and has recently emerged as a scaffolder regulating metabolic and autophagy pathways. However, the detailed protein-protein interactions linking FKBP51 to autophagy upon metabolic challenges remain elusive. We performed mass spectrometry-based metabolomics of FKBP51 knockout (KO) cells revealing an increased amino acid and polyamine metabolism. We identified FKBP51 as a central nexus for the recruitment of the LKB1/AMPK complex to WIPI4 and TSC2 to WIPI3, thereby regulating the balance between autophagy and mTOR signaling in response to metabolic challenges. Furthermore, we demonstrated that MBH FKBP51 deletion strongly induces obesity, while its overexpression protects against high-fat diet (HFD) induced obesity. Our study provides an important novel regulatory function of MBH FKBP51 within the stress-adapted autophagy response to metabolic challenges.

neuroscience↗