In contrast to their similar brain abnormalities, new-born mice deficient in Apa

Question

In contrast to their similar brain abnormalities, new-born mice deficient in Apaf1 or caspase-9 have distinctive abnormalities in their paws. Apad1-deficient mice fail to eliminate the webs between their developing digits, whereas caspase-9-deficient mice have normally formed digits (Fig-Q18-1). If Apaf1 and caspase-9 function in the same apoptotic pathway, how is it possible for these deficient mice to differ in web-cell apoptosis?

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Casp9 Apaf1 newborn Figure 018-1 Appearance of paws in Apafi and Caspg mice relative to normal newborn mice (Problem 18-6). From H. Yoshida et a Cel 94:739-750, With permission from Elsevier

Explanation / Answer

This follows an intrinsic apoptotic pathway

In this pathway, the cytochrome C is released in the cytosol. The cytochrome C which is now free in the cytoplasm binds to the Apaf (Apoptosis protease adaptor factor). Apaf then binds to procaspase 9 and initiates it. This leads to the formation of active caspase 9. Caspase 9 now cleaves and activates the other caspases which leads to and initiate apoptosis.

In the present case, the absence of Apaf-1 in Apaf-1 deficient mice, leads to the complete abasence of procaspase activation and hence the formation of caspase is also inhibited. Thus apoptosis is also absent and hence the Apaf-1 deficient mice fails to eliminate the webs between their developing digits.

Secondly, in the caspase-9 deficient mice, only caspase -9 is absent, while the adaptor protein Apaf-1 is present. Thus, the Apaf-1 can bind to a procaspase and produce or activate a new caspase-9. This leads to apoptosis of webs between digits and hence these mice have normally formed digits.

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