Force driven biological processes have long puzzled biologists. Little is known about how forces impact development of an organism. C. elegans provides a good in vivo system to study such a process. C. elegans embryonic elongation is driven by two forces i.e. actomyosin contractility and the tension provided by muscle contraction. We previously reported that the latter recruits GIT-1 to hemidesmosomes (HD), which in turn facilitates further elongation by activating proteins such as
pak-1 (Nature 471, 99-103, 2011). Whereas muscle-defective embryos are paralyzed and arrest at 2-fold (Pat phenotype),
git-1 null mutants are viable, suggesting that another pathway acts in parallel to the
git-1/pak-1. To identify genes involved in parallel pathways, we performed an enhancer RNAi screen to look for Body Morphology Defects (BMD) and 2-fold arrest in
git-1(
tm1962) animals. We found almost 100 candidates belonging to different cellular complexes. Genes such as
dnc-1,
arp-1,
cap-1 and
farl-11 give 80% 2-fold arrest and encode Dynein/dynactin subunits or regulators. To define their in elongation we combined
git-1(
tm1962) temperature sensitive (ts) alleles
egl-50(
n1046) and
dnc-1(
or404) (
egl-50 is another name for
arp-1) as dynein/dynactin alleles have early maternal effect lethality. An
egl-50(
n1086ts);
git-1(
tm1962) double mutant is viable at 15 deg C, but gives 70 % 2-fold arrest and 30% arresting earlier. Similar results were found for a
dnc-1(
or404ts);
git-1(
tm1962) double combination. Why do
egl-50;
git-1 embryos arrest at 2-fold? What structures are affected? To answer the question I created a library of markers in
egl-50;
git-1 background to look for structural and dynamic defects. We did not observe any major organization defects of actin cytoskeleton. Using the HD marker LET-805::GFP (CRISPR construct) in
egl-50;
git-1, I found multiple HD structural defects, such as thickened HDs, locally disrupted or bifurcated HDs, and more rarely detached HDs. To define the cause for this defect, I used FRAP analysis of LET-805::GFP, revealing three kinds of Mobile Fractions in
egl-50;
git-1 mutants, which could be similar, lower or higher than wild-type. I hypothesize that a higher mobile fraction makes the HD brittle, while a lower mobile fraction leaves HDs susceptible to not withstand the increasing muscle tension. Moreover, our data suggest that the Dynein/dynactin complex is essential to transport HD material.