At stages 13-14, approximately 40% of muscles are normal in mutant embryos, approximately 50% have abnormal projections and approximately 10% are rounded. Most muscles recover as embryogenesis proceeds in the mutant embryos, such that at stage 16, more than 80% of muscles are normal, while the remainder either have abnormal projections or are rounded.

Muscle VL1 exhibits abnormal morphology in approximately 50% of cases in Grip^ex36 embryos, either occasionally showing a rounded morphology or, more commonly, failing to span the entire abdominal segment.

Grip^ex36 mutants exhibit abnormal muscle patterning.

Grip^ex36 mutants show defects in ventrolateral muscle (VLM) morphogenesis. Instead of forming a single polarized muscle projection, the VLMs of Grip^ex36 mutants frequently send out two or more projections in essentially randomized directions. When the

muscle guidance period ceases, these VLMs typically form ball-like structures that extend over only about half of a hemisegment without reaching their target tendon cell. Lateral transverse muscles (LTMs) appear unaffected.

Expression of Grip^{Δ1-3.Scer\UAS}, under the control of Scer\GAL4^twi.PG leads to very strong defects in lateral transverse muscles (LTMs) Grip^ex36 and Grip^ex36/+ backgrounds. LTM defects include splitting into multiple projections, bending away from their target tendon cells and forming aberrant, integrin positive attachments in ectopic positions. These defects appear qualitatively very similar when scored in embryos or in larvae. Scer\GAL4^twi.PG>Grip^{Δ1-3.Scer\UAS} expression in a Grip^ex36 or Grip^ex36/+ background results in slight ventrolateral muscle (VLM) defects.

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. Affected VLMs position themselves randomly more at either the anterior or posterior end of the segment borders. IN weaker cases, while still attached to both segment borders, the mutant VLMs appear irregularly shaped and do not align in register at the segment borders. Over 95% of all VLMs 6/7 are affected 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.

Grip^ex36 has ventral longitudinal muscle cell phenotype, enhanceable by ed[+]/ed^1X5

Grip^ex36 has ventral longitudinal muscle cell phenotype, enhanceable by ed^UAS.cBa/Scer\GAL4^twi.PG