Value Proposition
· Conditional TrkB knockout capability: Floxed TrkB alleles enable precise spatial and temporal control over TrkB deletion when combined with Cre recombinase systems
· Tissue-specific targeting: Allows researchers to delete TrkB in specific cell types or brain regions while preserving function elsewhere
· Developmental stage control: Enables TrkB knockout at chosen developmental stages or in adult animals, avoiding early lethality issues
· BDNF pathway precision: Provides targeted approach to study TrkB function in specific neural circuits relevant to learning, memory, and psychiatric disorders
· Versatile research platform: Compatible with extensive library of existing Cre driver lines for diverse experimental applications
· Disease modeling applications: Enables creation of cell-type specific TrkB loss models relevant to depression, anxiety, and neurodegenerative diseases
Unmet Need
Researchers studying TrkB neurotrophin signaling face limitations with conventional knockout approaches that eliminate TrkB function throughout development and across all tissues, making it difficult to determine cell-type specific or adult-specific roles. Traditional TrkB knockouts often result in early developmental defects that confound interpretation of adult nervous system functions. Current research tools cannot adequately address questions about TrkB function in specific neural populations or during developmental windows.
Technology Description
Researchers developed genetically modified mice with a targeted mutation in TrkB, harboring LoxP sites useful for Cre-mediated recombination to generate a null allele. When crossed with Cre recombinase-expressing mouse lines, the floxed TrkB sequences are excised specifically in Cre-expressing cells, resulting in complete elimination of TrkB function. This conditional approach allows researchers to control precisely where and when TrkB is deleted.
Stage of Development
These mouse strains have been validated.
Data Availability
· n/a
Publication
Liu, Y., Rutlin, M., Huang, S., Barrick, C.A., Wang, F., Jones, K.R., Tessarollo, L., and Ginty, D.D. Sexually dimorphic BDNF signaling directs sensory innervation of the mammary gland. Science, 338:1357-60, 2012. PMCID: PMC3826154
