Laminins are heterotrimeric molecules found in all basement membranes. In mammals, they have been involved in diverse developmental processes, from gastrulation to tissue maintenance. The Drosophila genome encodes two laminin a chains, one b and one g, which form two distinct laminin trimers. So far, only mutations affecting one or other trimer have been analysed. In order to study embryonic development in the complete absence of laminins, we mutated the gene encoding the sole laminin b chain in Drosophila, LanB1, so that no trimers can be made. We show that LanB1 mutant embryos develop until the end of embryogenesis. Electron microscopy analysis of mutant embryos reveals that the basement membranes are absent and the remaining extracellular material appears disorganised and diffuse. Accordingly, abnormal accumulation of major basement membrane components, such as Collagen IV and Perlecan, is observed in mutant tissues. In addition, we show that elimination of LanB1 prevents the normal morphogenesis of most organs and tissues, including the gut, trachea, muscles and nervous system. In spite of the above structural roles for laminins, our results unravel novel functions in cell adhesion, migration and rearrangement. We propose that while an early function of laminins in gastrulation is not conserved in Drosophila and mammals, their function in basement membrane assembly and organogenesis seems to be maintained throughout evolution. can serve as PS2 integrin ligands (Graner et al., 1998). This is further supported by studies showing that lamininW is not recruited to muscle attachment sites in embryos carrying a mutation in the aPS2 subunit affecting the RGD binding site (Devenport et al., 2007).Only mutations in the a subunits have been described in Drosophila so far. Null mutations in the LanA gene result in embryonic lethality with defects in somatic muscles, dorsal vessel (heart) and endoderm (Henchcliffe et al., 1993;Yarnitzky and Volk, 1995). The a 3,5 chain is also required for proper localisation of anteroposterior markers in the oocyte and for normal pathfinding of pioneer axons in the brain (Deng and RuoholaBaker, 2000; Garcia-Alonso et al., 1996). In addition, hypomorphic mutants and trans-heteroallelic combinations of LanA give rise to adult escapers that have disorganised rhabdomeres and display vein defects and wing blistering (Henchcliffe et al., 1993). Mutations in wb have wing blisters and defects in the dorsal vessel, trachea, muscles and rhabdomeres . Mutations in the laminin b subunit (encoded by Laminin B1, LanB1) or g subunit (encoded by laminin B2, lanB2) have not been characterised.In this work, we have isolated null mutations in LanB1, allowing the generation of embryos lacking all laminin function. These embryos develop until the end of embryogenesis, suggesting that in Drosophila, as it is the case in nematodes and contrary to mice, laminins are not required for early embryonic morphogenetic events. Our analysis of LanB1 loss reveals that laminins are required for accumulation of major EC...

We have studied several cell behaviour parameters of mutant alleles of fat (ft) in Drosophila imaginal wing disc development. Mutant imaginal discs continue growing in larvae delayed in pupariation and can reach sizes of several times those of wild-type. Their growth is, however, basically allometric. Homozygous ft cells grow faster than their twin cells in clones and generate larger territories, albeit delimited by normal clonal restrictions. Moreover, ft cells in clones tend to grow towards wing proximal regions. These behaviours can be related with failures in cell adhesiveness and cell recognition. Double mutant combinations with alleles of other genes, e.g. of the Epidermal growth factor receptor (DER) pathway, modify ft clonal phenotypes, indicating that adhesiveness is modulated by intercellular signalling. Mutant ft cells show, in addition, smaller cell sizes during proliferation and abnormal cuticular differentiation, which reflect cell membrane and cytoskeleton anomalies, which are not modulated by the DER pathway.