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Recombination Systems & Tools

Tamoxifen Inducible Cre

A temporal gene deletion system using CreERT2 fusion protein—Cre recombinase fused to a mutant estrogen receptor ligand-binding domain (ERT2). Without tamoxifen, CreERT2 is sequestered in the cytoplasm by HSP90 chaperones. Tamoxifen administration triggers nuclear translocation and LoxP recombination, enabling gene deletion at defined timepoints in adult animals.

Overview

Tamoxifen inducible Cre (CreERT2) is a temporal gene deletion system that fuses Cre recombinase to a mutant estrogen receptor ligand-binding domain (ERT2). This fusion protein remains sequestered in the cytoplasm by HSP90 chaperones until tamoxifen administration triggers nuclear translocation and LoxP recombination. This system enables gene deletion at defined timepoints in adult animals, bypassing embryonic lethality and avoiding developmental compensation mechanisms.

Mechanism of CreERT2 Activation

In the absence of ligand, the ERT2 domain binds HSP90 chaperone proteins, sequestering the CreERT2 fusion protein in the cytoplasm away from nuclear DNA. Tamoxifen (or its active metabolite 4-hydroxytamoxifen) binds to ERT2, displacing HSP90 and exposing a nuclear localization signal. CreERT2 translocates to the nucleus where Cre catalyzes recombination between LoxP sites, permanently deleting the floxed sequence. Recombination is heritable through subsequent cell divisions.

Tamoxifen Dosing and Administration

Common administration routes include intraperitoneal injection (75-100 mg/kg in corn oil, most common), oral gavage (similar dosing), or tamoxifen-containing chow (250-500 mg/kg diet for extended dosing). Typical protocols use 3-5 consecutive daily injections. Recombination efficiency varies by tissue and Cre driver line. Researchers should verify deletion efficiency in target tissues by PCR, qPCR, or immunoblotting.

Frequently Asked Questions

What are the advantages of CreERT2 over constitutive Cre?

CreERT2 enables temporal control, allowing gene deletion at defined timepoints after normal development. This bypasses embryonic lethality of essential genes, avoids developmental compensation that can mask adult phenotypes, enables comparison of early versus late gene deletion effects, and provides matched controls (same genotype with and without tamoxifen treatment).

How quickly does gene deletion occur after tamoxifen administration?

Recombination at the DNA level occurs within 24-72 hours after tamoxifen administration. However, protein turnover determines functional knockout kinetics. For stable proteins, complete depletion may take 7-14 days. For rapidly turning over proteins, functional effects can be observed within 2-3 days. Researchers should verify both DNA recombination and protein loss in target tissues.

Is there background Cre activity without tamoxifen?

Most CreERT2 systems show minimal leakiness (background activity without tamoxifen), but this varies by Cre driver line and tissue. Some CreERT2 lines show detectable background recombination (1-10%) in sensitive reporter assays. For critical experiments, include tamoxifen-only and Cre-only controls to quantify background activity. Second-generation ERT2 systems have reduced leakiness compared to original ER fusions.

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Related Terms

Inducible Cre (Cre-ERT2 / Tamoxifen)

A system that fuses Cre recombinase to a modified estrogen-receptor ligand-binding domain (ERT2), confining it to the cytoplasm until activation by tamoxifen, thus providing temporal control of recombination.

Cre-lox System

A bacteriophage P1-derived site-specific recombination technology that utilizes Cre recombinase to mediate genomic modifications at engineered LoxP sequences. This technology underpins conditional gene engineering approaches in mammalian genetics.

Conditional Knockout (cKO) Mouse Models

A genetically engineered mouse in which a specific gene can be selectively inactivated in chosen tissues, cell types, or developmental stages—enabling precise studies of gene function while avoiding embryonic lethality or systemic effects.

Temporal Control (Induction Windows, Dosing)

The activation or deactivation of a genetic modification at a specific time or during a defined developmental window. This strategy allows researchers to study gene function dynamically and distinguish developmental effects from later ones.

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