Mammalian puberty: a fly perspective.
Juan GuiradoJuan Carranza-ValenciaJavier MorantePublished in: The FEBS journal (2022)
Mammalian puberty and Drosophila metamorphosis, despite their evolutionary distance, exhibit similar design principles and conservation of molecular components. In this Viewpoint, we review recent advances in this area and the similarities between both processes in terms of the signaling pathways and neuroendocrine circuits involved. We argue that the detection and uptake of peripheral fat by Drosophila prothoracic endocrine cells induces endomembrane remodeling and ribosomal maturation, leading to the acquisition of high biosynthetic and secretory capacity. The absence of this fat-neuroendocrine interorgan communication leads to giant, obese, non-pupating larvae. Importantly, human leptin is capable of signaling the pupariation process in Drosophila, and its expression prevents obesity and triggers maturation in mutants that do not pupate. This implies that insect metamorphosis can be used to address issues related to the biology of leptin and puberty.
Keyphrases
- adipose tissue
- induced apoptosis
- weight loss
- metabolic syndrome
- insulin resistance
- signaling pathway
- endothelial cells
- type diabetes
- poor prognosis
- aedes aegypti
- cell cycle arrest
- fatty acid
- induced pluripotent stem cells
- drosophila melanogaster
- endoplasmic reticulum stress
- genome wide
- gene expression
- cell death
- mouse model
- epithelial mesenchymal transition
- oxidative stress
- bariatric surgery
- loop mediated isothermal amplification
- binding protein
- zika virus
- pluripotent stem cells
- skeletal muscle
- long non coding rna
- rare case
- quantum dots