| Summary: | AP Endonuclease 1 (Apex1) is a major player in the base excision repair (BER) pathway, which accounts for the majority of oxidative DNA damage repair in eukaryotic cells. Loss of Apex1 in developing vertebrate embryos, whether by artificial knockdown or genetic knockout, is lethal and halts development near the onset of gastrulation. To date, no one has successfully cultured Apex1 -/- cells from any source, suggesting its vital role for Apex1. Our lab has recently discovered
a regulatory relationship between Apex1 and the cAMP response element binding (Creb) complex in zebrafish and mice. Partial knockdown of Apex1 using morpholino oligonucleotides (MO) in zebrafish embryos leads to a diminution of transcript and protein of the Creb complex genes by 24 hours post-fertilization (hpf), as well as transcripts of some genes controlled by Creb. However, the means by which Apex1 controls the Creb complex, and thereby embryonic development, remain a
mystery.
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