All homozygous sima^j11B7 mutants are non-viable.

Clusters containing homozygous somatic clones of sima^j11B7 display defects during border follicle cell migration. First, the mutant cells are always detected in the leading cell in the cluster. In wild-type cells, there is alternative, competing leadership among the cells of a cluster. Furthermore, in cases in which there is more than one sima^j11B7-mutant cell within the same border cell cluster, only one mutant cell is detected to lead the cluster, whereas the other mutant cell is migrating with the rear of the cluster. During stage 9 of oogenesis, 80-90% of border cell clusters with sima^j11B7-mutant cells migrate faster than the corresponding anterior follicle cells, reaching the nurse cell and oocyte border prematurely. Moreover, sima^j11B7-mutant leading cells appear to be pulling the clusters forward more efficiently than wild-type leading cells, because there is an extension of the actin network between the leading sima^j11B7-mutant cell and the following cell. In contrast, the predominant phenotype observed during stage 10 of oogenesis is a delay of migration.