In contrast, surprisingly MV and PDV infection was enhanced. Antibody to b1 integrins was previously reported to have no effect on fusion activity of MV in Hela cells. However, viral antigen/infectivity levels were not examined. Antibodies to members of the tetraspans have been found to inhibit or enhance cell fusion depending on the virus, due to either physical separation of the virus fusion machinery from cell-cell contact areas or to inclusion of viral envelope proteins in the tetraspan complex. Furthermore, permissiveness of macrophages to MV using CD46 as a receptor is increased with formation of a complex of CD9, b1 integrins and CD46. It is therefore possible that anti-b1 integrin treatment is enhancing complex formation in a similar way in the Vero cell membrane allowing closer contact of MV and PDV H and F proteins with CD46 and proHB-EGF, respectively. It will be necessary to examine a range of integrin b1 function blocking antibodies to determine if they increase rather than reduce infection. ProHB-EGF is also a heparin binding molecule and binding to heparin could enhance infection. Heparinase and sodium chlorate treatments of Vero cells had no effect on released virus titre. However, inhibition of fusion occurred in treated cultures. The effect was less apparent in wtPDV infected cultures due to the more limited level of fusion compared to MV even in untreated cultures. We propose that binding of PDV to heparin or heparin like molecules associated with proHB-EGF would enhance F protein interaction with the cell membrane but this will require further LY294002 side effects investigation. In conclusion, we have confirmed that SLAM is used as a receptor by wtPDV and that the virus does not utilise CD46.The results also indicate that PVRL4 is also used as a receptor in common with MV, CDV and PPRV. This common second receptor may further increase the probability of cross species infection. The finding that wtPDV can use proHB-EGF as a low density receptor in Vero cells indicates that the binding site in the wtPDV H protein requires no or minimal change to utilise this receptor. It remains to be determined if this receptor has a role during PDV infection in the natural host but the lack of adaption required to infect Vero cells and the high conservation of the transmembrane sequence suggests that this is likely to be the case. The lineal descendants of each founder cell exhibit related developmental fates and similar cell cycle timing. Generation of the founder cells appears to be primarily under the control of maternal factors deposited into the oocyte prior to fertilization, many of which are uniquely specialized for founder specification. After maternal specification of the founder blastomeres, elaboration of the founder cell developmental program then comes under zygotic control. The progeny of the 8-cell stage E blastomere is a clone of 20 cells that constitute the entire intestine of the animal. Two GATA factors, END-1 and END-3, are expressed zygotically in the E blastomere and function somewhat redundantly for intestinal cell specification. Loss-of-function mutation in both end-1 and end-3 results in an E blastomere that does not produce intestinal cells, and instead produces muscle and epithelial cells.