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Abstract

Glial cells are the primary immune responders in the central nervous system, rapidly clearing degenerating tissue after injury, yet the molecular mechanisms driving this process remain unclear. Using an acute axotomy model in Drosophila, this study provides the first evidence that insulin-like signaling via the insulin-like receptor (InR) and its conserved downstream components is essential for effective glial clearance of axonal debris. InR signaling positively regulates the engulfment receptor Draper, and forced Draper expression partially rescues clearance defects caused by InR knockdown, highlighting insulin-like signaling as a critical regulator of innate glial immune responses and a potential mechanism for coordinating complex cellular events following CNS damage.

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