In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. The phenotype summarized below is for the parental line: Sst-IRES-Cre knock-in mice on a mostly C57BL/6;129S4 genetic background (Stock No. 013044). It should be noted that the phenotype of these C57BL/6NJ-congenic Sst-IRES-Cre knock-in mice (Stock No. 018973) could vary from that of the parental line from which it was derived. The phenotype below describes the parental line (Stock No. 013044).

The Sst-IRES-Cre knock-in allele (or SOM-IRES-Cre) has an internal ribosome entry site and Cre recombinase in the 3' UTR of the somatostatin locus (Sst). As such, the endogenous Sst promoter/enhancer elements direct cre expression to somatostatin-expressing neurons. While Sst-IRES-Cre was designed as a 3' knock-in allele, additional characterization indicates it has significantly diminished endogenous Sst expression - see details below. As such, researchers should consider using heterozygous AVP-IRES2-Cre-D mice and wildtype littermate controls in all their studies.
When Sst-IRES-Cre mice are bred with mice containing loxP-flanked sequences, Cre-mediated recombination will result in deletion of the floxed sequences in the Sst-expressing cells in the offspring.

In 2010, the donating investigator of Stock No. 013044 reported Cre recombinase activity is specific and efficient; largely recapitulating the endogenous somatostatin expression pattern with efficient recombination. They reported Cre recombinase activity is observed in somatostatin positive neurons (including dendritic inhibitory interneurons such as Martinotti cells and Oriens-Lacunosum-Moleculare (O-LM) cells). The donating investigator did not examine cre expression in tissues other than brain. Sst expression from the Sst-IRES-Cre allele was not evaluated. They also reported that homozygous mice were viable, fertile and normal in size, with no gross physical abnormalities or behavioral abnormalities.

Although Sst-IRES-Cre was designed as a 3' knock-in allele, additional characterization indicates it has significantly diminished endogenous Sst expression. Specifically, in 2016, unpublished research using Stock No. 013044 reported the Sst-IRES-Cre allele had diminished Sst RNA expression, and homozygous mice had abnormal locomotor activity (reduced in males during circadian cycle active phase, increased in females by the end of circadian cycle active phase). Heterozygous mice had partial recovery of Sst expression and normal behavioral responses. Furthermore, the findings of another group confirmed Sst-IRES-Cre imparts an allele dosage-dependent knock-down of endogenous Sst expression [Viollet et al. 2017 Front Endocrinol (Lausanne) 8:131 (PMID:28674519)]. Researchers researchers should consider using heterozygous Sst-IRES-Cre mice and wildtype littermate controls in their studies.

For characterization information of the Sst-IRES-Cre knock-in allele, see images at the Allen Institute for Brain Science website (Sst-IRES-Cre images).

If the recombinase activity pattern of this allele is further characterized by the Genetic Resource Science group at The Jackson Laboratory, such findings will be reported on the Mouse Genome Informatics (MGI) Allele Detail entry (Sst^{tm2.1(cre)Zjh}). This same information would also be found searching the MGI Recombinase Activity database.