The engrailed gene acts early in Drosophila embryogenesis and plays an essential role in the processes that establish and maintain the repeating segmental pattern. To begin molecular analysis of the role of the engrailed gene in embryonic pattern formation, we used a chromosomal walk to clone genomic sequences that encompass the locus, and have physically mapped the positions of 15 engrailed mutations. The positions of engrailed rearrangement mutations indicate that the engrailed complementation unit includes a minimum of 70 kb. The locus can be divided into two regions. Rearrangement mutations interrupting the centromere proximal 50 kb of the locus result in embryonic lethality while mutants altered in the distal 20 kb of the locus survive to show morphological abnormalities in several adult segments. It appears that long-range cis interactions play a role in the function of the engrailed gene.
Induced by starvation, the development of fruiting bodies by Myxococcus xanthus on glass and plastic surfaces under a layer of liquid was followed microscopically. Calcium ions and a neutral pH were required for development of a Myxococcus strain that grew dispersed in liquid culture. Initially asymmetric aggregates later became round, and sporulation followed aggregation.
A set of developmental mutants have been examined that behave as if defective in cellular interactions necessary for the formation of myxospores during fruiting body development. Sporulation is rescued in these mutants if they are mixed with wild-type cells. Complementation experiments with whole cells divide the mutants into four groups (A, B, C, and D). Mutants of group A appear to be less responsive to starvation, a condition that normally initiates development. Mutants of group D respond to starvation but fail to synthesize myxobacterial hemagglutinin, a protein normally synthesized midway in development. Mutants of groups B and C respond to starvation and synthesize hemagglutinin, but they can be distinguished genetically. Group C mutations all map in a single cluster near insertion omega 1519 of transposon Tn5, which is distant from group B mutations. Thus, each group represents a different defect in development. All of the mutants are induced to sporulate by glycerol. Therefore, we argue that sporulation during fruiting body development depends on several prior interactions between cells.
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