It is a membrane protein It is a bridging molecule that binds PS TTR-52 clusters around apoptotic cells, because It is a membrane protein It is a bridging molecule that binds PS It is made in apoptotic cells It is a receptor for PS None of above

Which of the following is important for TTR-52 activity The signal sequence The transthyretin-like domain Its ability to bind PS Its ability to bind CED-1 All of the above

TTR-52 was found to act in the ced-1 pathway, because It can bind CED-1 Inactivation of ttr-52 does not enhance the engulfment defect of the ced-1 mutant It is a bridging protein that binds PS It co-localizes with CED-1 to apoptotic cells None of the above

In Figure 7, ttr-52(lf) can block the missing cell phenotype caused by loss of tat-1, because ttr-52 is required to recognize living cells with surface-exposed PS ttr-52 is required to externalize PS in the missing cells ttr-52 is required to recognize a new “eat-me” signal on the living cells ttr-52 can kill these cells directly None of the above

Based on the paper, the following is observed CED-1 binds to apoptotic cells before TTR-52 does TTR-52 binds to apoptotic cells before CED-1 does CED-1 binds to surface-exposed PS before TTR-52 does TTR-52 binds to surface-exposed PS before PSR-1 does None of the above