During cell stress, the transcription and translation of immediate early genes 
are prioritized, while most other messenger RNAs (mRNAs) are stored away in 
stress granules or degraded in processing bodies (P-bodies). TIA-1 is an 
mRNA-binding protein that needs to translocate from the nucleus to seed the 
formation of stress granules in the cytoplasm. Because other stress granule 
components such as TDP-43, FUS, ATXN2,SMN, MAPT, HNRNPA2B1, and HNRNPA1 are 
crucial for the motor neuron diseases amyotrophic lateral sclerosis (ALS)/spinal 
muscular atrophy (SMA) and for the frontotemporal dementia(FTD), here we studied 
mouse nervous tissue to identify mRNAs with selective dependence on Tia1 
deletion. Transcriptome profiling with oligonucleotide microarrays in comparison 
of spinal cord and cerebellum, together with independent validation in 
quantitative reverse transcriptase PCR and immunoblots demonstrated several 
strong and consistent dysregulations. In agreement with previously reported TIA1 
knock down effects, cell cycle and apoptosis regulators were affected markedly 
with expression changes up to +2-fold, exhibiting increased levels for Cdkn1a, 
Ccnf, and Tprkb vs.decreased levels for Bid and Inca1 transcripts. Novel and 
surprisingly strong expression alterations were detected for fat storage and 
membrane trafficking factors, with prominent +3-fold upregulations of Plin4, 
Wdfy1, Tbc1d24, and Pnpla2 vs. a −2.4-fold downregulation of Cntn4 transcript, 
encoding an axonal membrane adhesion factor with established 
haploinsufficiency.In comparison, subtle effects on the RNA processing machinery 
included up to 1.2-fold upregulations of Dcp1b and Tial1. The effect on lipid 
dynamics factors is noteworthy, since also the gene deletion of Tardbp (encoding 
TDP-43) and Atxn2 led to fat metabolism phenotypes in mouse. In conclusion, 
genetic ablation of the stress granule nucleator TIA-1 has a novel major effect 
on mRNAs encoding lipid homeostasis factors in the brain, similar to the fasting 
effect.