Where do blind mice come from? - briefly
Blind mice originate from genetic mutations that eliminate functional eyes, propagated through selective breeding of laboratory strains such as albino or C57BL/6 lines.
Where do blind mice come from? - in detail
Blind laboratory mice that lack functional vision arise from spontaneous genetic mutations identified in breeding colonies. The first documented sightless strain appeared in the early 20th century when a mouse pup exhibited a white, cataract‑like eye and failed to respond to visual cues. Genetic analysis later linked the phenotype to a recessive allele in the Pde6b gene, now known as the rd1 mutation. This mutation disrupts phosphodiesterase activity in photoreceptors, causing rapid degeneration of the retina and complete blindness shortly after birth.
Subsequent breeding programs isolated the rd1 allele and incorporated it into standard inbred backgrounds such as C57BL/6 and BALB/c. Researchers maintained the trait by homozygous breeding, ensuring that each generation produced offspring devoid of functional photoreceptors. Additional blind models emerged from targeted gene knockouts (e.g., Rho‑knockout, Crx‑null) and chemical mutagenesis screens, expanding the repertoire of vision‑deficient mice for neuroscience and ophthalmology.
Current sources for these animals include major mouse repositories:
- The Jackson Laboratory (stock numbers JAX: 000058 for rd1, JAX: 004292 for Rho‑knockout)
- Charles River Laboratories (various blind strains listed under “Vision‑Impaired Models”)
- European Mutant Mouse Archive (EMMA) (catalogue entries for CRISPR‑generated blind alleles)
Breeding practices follow strict Mendelian inheritance: two heterozygous carriers produce a 25 % chance of blind offspring per litter, while homozygous pairs yield 100 % blind progeny. Maintaining the phenotype requires regular genotyping to confirm the presence of the causative mutation and to avoid accidental outcrossing that could reintroduce functional alleles.
In summary, sightless mice originate from naturally occurring or engineered genetic defects that eliminate retinal function. Their propagation relies on controlled breeding within established inbred lines, and they are distributed worldwide through specialized animal supply facilities for experimental use.