The TRIM37 gene encodes a peroxisomal protein of unknown function. Mutations in 
TRIM37 underlie mulibrey nanism, a rare autosomal recessively inherited disorder 
with severe growth failure of prenatal onset, constrictive pericardium, 
hepatomegaly and characteristic dysmorphic features. Eleven mulibrey 
nanism-associated mutations have been identified. We here characterised TRIM37 
further by mapping the transcription initiation site and promoter region as well 
as by analysing splice variants. By primer extension analysis, several 
transcription initiation sites were localised to a region between -246 and -373 
relative to the ATG codon for translation initiation. Basal promoter activity 
was mapped within 600 nucleotides upstream from the translation initiation site 
using promoter-luciferase reporter constructs. Several alternative splice 
variants of TRIM37 exist in databases. Most of these predict non-functional 
protein products, are expressed at low levels and are thus likely to be targets 
for nonsense-mediated mRNA decay. A novel splice variant, TRIM37b, with an 
alternative termination codon and 3'untranslated region (UTR) transcribed from 
an exon 16 kb downstream from exon 24, predicts an identical protein product 
with the previously identified transcript, TRIM37a. As seen by Northern blot 
analysis and quantitative real-time PCR, both transcripts are highly expressed 
in testis, whereas in other tissues TRIM37a is prominent. The 3'UTR of the PPM1E 
gene in the opposite strand overlaps TRIM37b. These data suggest that TRIM37 
expression is regulated by several mechanisms: through nonsense surveillance of 
non-functional transcripts, as well as through 3'UTR regulatory sequences and/or 
naturally occurring antisense RNAs especially in testis.