Nanoscale mechanisms limiting non-basal plasticity in magnesium

Dislocations of the 〈c+a〉type are widely recognized as the primary defects limiting the ductility of magnesium. While their glide can be activated in small magnesium crystals under high flow stresses, our in-situ transmission electron microscopy compression tests, conducted over a large strain range, reveal that 〈c+a〉dislocation plasticity becomes inactive following initial activation, leading to dislocation avalanches and subsequent deformation twinning. Initially, pyramidal II slip mediated by 〈c+a〉dislocations accommodates plastic deformation in caxis-oriented magnesium pillars under compression. However, as deformation progresses, interactions among dislocations increasingly impede further glide and prevent surface annihilation. Correlative atomistic simulations indicate that this limited dislocation plasticity arises from the formation of basal I1 and I2 stacking faults, generated by interactions between glissile pyramidal II dislocations. The restricted motion of 〈c+a〉dislocations consequently results in stress accumulation, which triggers dislocation avalanches and deformation twinning. This deformation behavior fundamentally differs from the typical dislocation starvation or exhaustion mechanisms observed in small-scale plasticity, offering novel insights into plasticity and work hardening in bulk magnesium.