Intrinsic and damage-induced JAK/STAT signaling regulate developmental timing by the Drosophila prothoracic gland

Area of Science:

• Developmental Biology
• Molecular Biology
• Immunology

Background:

• Development requires precise timing but must adapt to external factors like damage.
• The Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway mediates damage responses and is crucial for normal development.
• The intersection of inflammatory and developmental roles of JAK/STAT signaling remains unclear.

Purpose of the Study:

• To investigate whether inflammatory and developmental roles of JAK/STAT signaling intersect.
• To determine the role of JAK/STAT signaling in the development of the prothoracic gland (PG).
• To understand how damage signaling affects metamorphosis onset via the PG.

Main Methods:

• Studied JAK/STAT signaling activity during prothoracic gland (PG) development in Drosophila.
• Manipulated JAK/STAT signaling levels (reduction and hyperactivation) in the PG.
• Investigated the effects of tissue damage and tumors on PG JAK/STAT activity and metamorphosis.
• Analyzed the expression of the JAK/STAT target gene Apontic.

Main Results:

• JAK/STAT signaling is active during PG development, controlling metamorphosis onset.
• Reduced JAK/STAT signaling led to smaller PG size and advanced metamorphosis.
• JAK/STAT hyperactivation resulted in PG hypertrophy and delayed metamorphosis.
• Tissue damage and tumors activated JAK/STAT in the PG, delaying metamorphosis partly via Apontic induction.

Conclusions:

• JAK/STAT signaling's developmental role in the PG is co-opted by damage signaling to regulate metamorphosis.
• Systemic effects of damage and cancer can disrupt hormonally controlled development and transitions.
• Findings in Drosophila offer insights into conserved mechanisms of damage-induced developmental interference.