Mechanisms Causing Loss Of Chordate Features In Tunicate Adults

The loss of chordate features in tunicates (specifically ascidians) is a highly regulated, rapid, and destructive process triggered when the larva settles. The primary mechanisms are:

1. Programmed Cell Death (Apoptosis): This is the main driver. Once the larva attaches to a substrate, a cascade of genetic signals initiates apoptosis in the cells of the tail, notochord, and the larval dorsal nerve cord.
2. Phagocytosis and Resorption: As these structures undergo apoptosis, they are rapidly broken down and "eaten" by phagocytic cells. The nutrients and materials from these "advanced" larval structures are recycled to build the new "simpler" adult body parts, like the enlarged pharynx (branchial basket) and gonads.
3. Nervous System Reorganization: The larval brain (sensory vesicle with an otolith for balance and an ocellus for light) degenerates. The dorsal hollow nerve cord is completely destroyed. A new, much simpler adult cerebral ganglion develops, which is just a solid nerve cluster sufficient for controlling the filter-feeding and spawning activities of the sessile adult.
4. Body Axis Rotation: The entire body plan reorients. The larva attaches by its "chin" (adhesive papillae). The mouth, which was internal, rotates 90-180 degrees to become the upward-facing incurrent siphon, and the atrial opening becomes the excurrent siphon.