G. Sohl et al., A 2ND ALTERNATIVE TRANSCRIPT OF THE GAP JUNCTION GENE CONNEXIN32 IS EXPRESSED IN MURINE SCHWANN-CELLS AND MODULATED IN INJURED SCIATIC-NERVE, European journal of cell biology, 69(3), 1996, pp. 267-275
Four connexin32 (Cx32) cDNA clones isolated from a rat sciatic nerve c
DNA library differ in the nucleotide sequence of their 5' untranslated
region (UTR) from the corresponding Cx32 cDNA clones previously chara
cterized from liver. The new Cx32 5'UTR sequence detected in the sciat
ic nerve cDNA clones is identical to one previously found in the 6.5 k
b intron of the murine Cx32 gene, Using primer extension and S1 nuclea
se protection analysis, we determined the transcriptional starting poi
nt of this new alternative Cx32 transcript expressed in the sciatic ne
rve. This starting point is located 444 bp (409 bp) upstream of exon2
in a region previously described as an intron of the Cx32 gene in the
rat (and mouse) genome, respectively. The alternative exon1B comprises
99 bp in rat, but 97 bp in the mouse genome, and is spliced to the sa
me exon2 acceptor site also used for splicing of exon1 in liver. Both
transcripts are likely to code for the same Cx32 protein whose reading
frame is located in exon2. The putative promoter region, upstream of
the alternative exon1B, contains a TATAAA moth and has been sequenced
and noticed before by Miller et al. (Biosci. Rep. 8, 455-464, (1988)).
The alternative exon1B transcript is highly expressed in the sciatic
nerve, (i.e. Schwann cells) and very low in liver (i.e. hepatocytes).
its expression is regulated after sciatic nerve injury. The time cours
e of expression was similar to previously established myelin genes aci
d, therefore, we suggest that the expression of the alternative exon1B
Cx32 transcript is related to the process of myelination. Very recent
ly we have characterized another alternative Cx32 exon1A which is tran
scribed in mouse embryonic stem cells but not in the sciatic nerve (Da
hl et al., submitted for publication, 1995). Thus, the murine Cx32 gen
e is likely to be regulated by three alternative promoters that appear
to be activated in a cell type-specific manner.