HYOBRANCHIAL APPARATUS OF SPELERPES 543 



generally taken for granted, but it is largely a new structure 

 which has developed from the old in a most curious way. At 

 the stage which Mrs. Wilder calls 'incipient premetamorphic,' 

 when the first signs of approaching metamorphosis appear, I 

 find on the ventral surface of the first epibranchial for a short 

 distance posterior to the insertion of the ceratohyoideus internus 

 and the origin of the constrictor arcuus primi, a slight swelling 

 of the cartilage and conspicuous thickening of the perichron- 

 drium with a number of mitoses (figure 32). This is the anlage 

 of a new portion of the epibranchial. Dorsal to it, a very slight 

 raggedness of the hyaline matrix is the first indication of the 

 degeneration soon to take place. The laying down of new car- 

 tilage by the chondrioblasts and degeneration of the old matrix 

 continues slowly until the time when the animal enters into the 

 true 'metamorphic' period. By that time the new sprout has 

 been cut off from the larval first epibranchial for a short dis- 

 tance and appears as a ventral fork of that cartilage with the 

 old matrix degenerating behind it (fig. 36). Posterior to the 

 tip of the new epibranchial, the old one is still quite typically 

 larval. From now on, these phenomena continue rapidly. The 

 new epibranchial grows ventroposteriorly, apparently by pro- 

 liferation of cells from the perichondrium and frequent mitoses 

 especially near the tip (fig. 3), and the old epibranchial breaks 

 down by an anteroposterior wave of degeneration. The first 

 sign of degeneracy is seen in a raggedness of the haline matrix; 

 then the spaces in the cartilage become filled with leucocytes 

 (phagocytes) which eventually eat away all the old tissue. 

 Thus, by the end of the metamorphic period, the new epibran- 

 chial has very nearly its adult proportions and position, and the 

 posterior two-thirds of the larval first epibranchial is almost 

 indistinguishable from a blood-vessel, except for occasional re- 

 maining bits of hyaline matrix (figs. 42 and 47). 



So, throughout the whole visceral skeleton new pieces develop 

 from old by a proliferation of and subsequent formation of car- 

 tilage by chondrioblasts; old ones disappear by a degeneration of 

 matrix and final consumption by phagoctyes, and permanent 

 cartilages change their shape and position by partial degeneration 

 and outgrowth of new tissue in the same ways. 



