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Retrograde Signaling That Regulates Synaptic Development and Function at the Drosophila Neuromuscular Junction

2006; Elsevier BV; Linguagem: Inglês

10.1016/s0074-7742(06)75012-7

2162-5514

Guillermo Marqués, Bing Zhang,

Physiological and biochemical adaptations

This chapter discusses the molecular mechanisms of retrograde signaling at the Drosophila neuromuscular junction (NMJ). Retrograde signaling regulates synaptic development and plasticity and maintains homeostatic regulation of synaptic strength over the muscle fiber. However, the precise mechanisms used to trigger retrograde signals and modify presynaptic terminals are not fully understood. The only identified retrograde signaling molecule at the larval NMJ is the bone morphogenetic protein (BMP) encoded by the gene glass bottom boat (Gbb). Two types of BMP receptors—the type-I, saxophone (Sax) and thick veins (Tkv), and the type-II, wishful thinking (Wit)—transduce the retrograde signal in the motoneurons through the downstream effectors medea and “mothers against decapentaplegic (dpp)” (Mad). A working model proposes that the muscle cell secretes Gbb, either constitutively or in response to insufficient muscle contraction. Gbb binds to presynaptic BMP receptors, thereby leading to the activation of the receptors and phosphorylation of Mad. The motoneuron responds to this pathway activation by increasing synaptic size and the amount of neurotransmitter released.