RNA localization pathways direct numerous mRNAs to distinct subcellular regions 
and affect many physiological processes. In one such pathway the 
tumor-suppressor protein adenomatous polyposis coli (APC) targets RNAs to cell 
protrusions, forming APC-containing ribonucleoprotein complexes (APC-RNPs). 
Here, we show that APC-RNPs associate with the RNA-binding protein Fus/TLS 
(fused in sarcoma/translocated in liposarcoma). Fus is not required for APC-RNP 
localization but is required for efficient translation of associated 
transcripts. Labeling of newly synthesized proteins revealed that Fus promotes 
translation preferentially within protrusions. Mutations in Fus cause 
amyotrophic lateral sclerosis (ALS) and the mutant protein forms inclusions that 
appear to correspond to stress granules. We show that overexpression or mutation 
of Fus results in formation of granules, which preferentially recruit APC-RNPs. 
Remarkably, these granules are not translationally silent. Instead, APC-RNP 
transcripts are translated within cytoplasmic Fus granules. These results 
unexpectedly show that translation can occur within stress-like granules. 
Importantly, they identify a new local function for cytoplasmic Fus with 
implications for ALS pathology.