Previous studies of TRCF revealed a molecular architecture incompatible with UvrA binding, leaving its recruitment mechanism unclear. In bacteria, the transcription-repair coupling factor (TRCF also known as Mfd) SF2 ATPase recognizes RNA polymerase stalled at a site of DNA damage, removes the enzyme from the DNA, and recruits the Uvr(A)BC nucleotide excision repair machinery via UvrA binding. Transcription-coupled DNA repair targets DNA lesions that block progression of elongating RNA polymerases. Our results show that the Ai38 reporter mouse provides a flexible method for targeted expression of GCaMP3. In the retina, Ai38 allowed imaging spontaneous calcium waves in starburst amacrine cells during development, and light-evoked responses in ganglion cells in adult tissue. GCaMP3 signals were rapid, compared with virally expressed GCaMP3 and synthetic calcium indicators. In the primary visual cortex, visually evoked GCaMP3 signals showed normal orientation and direction selectivity. Crossing Ai38 with appropriate Cre mice produced robust GCaMP3 expression in defined cell populations in the retina, cortex, and cerebellum. Here, we developed a genetic reporter mouse, Ai38, which expresses GCaMP3 in a Cre-dependent manner from the ROSA26 locus, driven by a strong CAG promoter. However, these methods are invasive and provide inhomogeneous and nonstationary expression. GCaMP3 can be expressed using various gene delivery methods, such as viral infection or electroporation.
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