Grip^ex122/Y mutant animals exhibit abnormal patterning of the ventral longitudinal muscles (VLMs). The VLMs of the mutants appear rounded instead of stretched between the attachment sites at the segment borders. Hemizygous and Grip^ex122/Grip^ex36 animals develop into larvae which maintain the defective VLM pattern seen in embryos. Within these animals, the embryonically affected muscles grow and elongate throughout larval development. No sign of muscle degeneration is recognisable. affected VLMs produce ectopic intrasegmental attachments. These attachments form at the inner layer of muscles and not at the epidermis. Both in embryos and in larvae, even the most affected mutant VLMs form multiple extensions. Defective VLMs also have normal organisation of the contractile apparatus. Adult escapers show a shrunken abdomen and defective head posture. No other defects, in particular no signs of general impairment of cell adhesion, are observed in the animals. The development of the muscle 12 precursor is abnormal, exhibiting defective guidance behaviour. At stage 13 cellular extensions are seen the protrude in the wrong direction, as compared to wild-type. Moreover, precursors cells appear bipolar, forming extensions in both anterior and posterior directions. Cell extensions often appear collapsed, or of developed, they miss their proper target sites at the segment borders.