Heat shock transcription factor 4 (HSF4) is primarily expressed in the ocular lens and plays a critical role in lens formation and differentiation. HSF4 was also found to be expressed in mature CD4+, CD8+, and CD3+ (T cell receptor) thymocytes, muscles, and neurons. Mutations in the Hsf4 gene are associated with congenital cataracts. Loss of HSF4 induces cellular senescence and delays tumorigenesis in vivo. These Hsf4-deficient mice have an enhanced green fluorescent protein/loxP-flanked neomycin cassette inserted into exon 1 of the heat shock transcription factor 4 (Hsf4) gene, resulting in loss of endogenous Hsf4 expression. Homozygous mice are viable and fertile, but do demonstrate microphthalmia and complete lens opacity in both eyes by ~3-4 weeks of age. Neither HSF4a and HSF4b isoforms are measurable in the lens of the homozygous mice. EGFP expression was detectable in the lens by confocal microscopy. Hsf4-deficient mice may be useful for studying the regulatory role of HSF4 in ocular lens development.

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Hsf4-deficient mice harbor an EGFP-floxed neomycin cassette that was inserted in exon 1 of the Hsf4 gene, resulting in loss of endogenous Hsf4 expression. These mice may be useful for studying eye lens development.

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