Figure 7.

The actin-binding CaMKIIβ′ is the dominant splice variant in rat pancreatic islets. Products from RT-PCR with CaMKIIβ-specific primers flanking the variable region were separated by agarose gel electrophoresis. Grayscale-inverted images of ethidium bromide stains are shown. (A) Cortex and whole brain was analyzed at different days after birth (pn), as indicated. Assignment of CaMKIIβ splice variants to the bands was based on length and (Brocke et al. 1995). (B) CaMKIIβ splice variants were detected in brain, skeletal muscle, and pancreatic islets, but not in heart of adult rats. The variant detected in skeletal muscle corresponded in length to CaMKIIβM (and contained exon v1 sequences based on SacII digest; our unpublished data); the major variant detected in islets corresponded to CaMKIIβ′. (C) The RT-PCR product from rat pancreatic islets was digested with enzymes that cut in different variable exons (−, no enzyme; v1, SacII; v3, BamHI; and v4, MseI). Resistance only to MseI digest indicates lack of exon v4, corresponding to CaMKIIβ′. SacII and BamHI digests yielded band of similar length, as expected for β′ PCR amplificates (6 base pairs difference); the same digests of β amplificates would differ by 49 base pairs. Identity of the RT-PCR product as β′ was also confirmed by direct sequencing (our unpublished data).