A bgal cell population in this pattern was seen at all postnatal stages, though the number of labelled cells appears to decrease with age. colocalisation of b-galactosidase with s100b in cells present in close proximity to Purkinje cells at both P10 and P21 supports the hypothesis that some Bergmann glia respond to a Wnt/b-catenin signal during development. Expression of LacZ mRNA identified at all stages except for P21 supports a potential role for Wnt/b-catenin signalling during development, and would suggest that residual bgalactosidase protein has been identified at P21. Interestingly, the lack of b-galactosidase expression at the ventricular zone at E14.5 indicates that Wnt/b-catenin signalling is not involved in the birth of the Bergmann glia but may be potentially involved in its further development and maturation. This is consistent with the postnatal dynamic transformation of Bergmann glia alongside dendritogenesis and synaptogenesis of Purkinje cells and suggests a possible role for Wnt/b-catenin in this process. Cells are constantly exposed to a variety of endogenous and exogenous agents that form bulky adducts on DNA, including by the environmental carcinogens ultraviolet light and benzopyrene. These lesions are problematic because they interfere with many DNA metabolic processes, including transcription and DNA replication. Though these lesions can be removed from the genome through the process of nucleotide excision repair, the lack or inefficiency of this repair process may lead to cell death, mutagenesis, or to abnormal cell proliferation. To combat DNA damage, eukaryotic cells have evolved DNA damage checkpoint responses, which are signal transduction pathways that respond to DNA damage by delaying cell cycle progression to allow time for DNA repair. In organisms ranging from yeast to man, the phosphoinositide-3-kinase-related protein kinase ATR plays a primary role in the initial response to bulky DNA adducts and to problems that arise during replication of adducted bases. A critical substrate of ATR is the signal transducing kinase Checkpoint Kinase 1. Upon phosphorylation and activation by ATR, Chk1 phosphorylates additional protein factors that impact DNA repair and cell cycle progression, such as the protein phosphatase Cdc25A. Phosphorylation of Cdc25A by Chk1 triggers its ubiquitination and degradation by the proteasome, therefore preventing Cdc25A from dephosphorylating and activating the cyclin-dependent Compound Library kinases that drive cell cycle progression.