Fig. 8.

Temporal modulation of miR-101a/fosab genetic circuit controls heart regeneration. In response to injury, miR-101a levels are reduced, enabling fosab expression to increase. This enhanced fosab expression promotes CM proliferation. However, between 7 and 14 dpa, miR-101a levels are significantly elevated, leading to repression of fosab activity. This decline in Fosab protein attenuates scar tissue deposition. miR-101a regulation of fosab during these defined regeneration intervals is crucial for normal heart regeneration.