J Craig's research while affiliated with University of Ottawa and other places

... Given that Hh and Wnt signalling are essential in neural differentiation, and that Nek2 acts as a regulator of both pathways, we sought to explore the role of Nek2 in neural differentiation using P19 embryonal carcinoma cells. These cells can be differentiated towards neurons and astrocytes in the presence of retinoic acid (RA) [33][34][35][36][37], which affects Wnt [3,5,38,39] and Hh [37,40] signalling. Herein, we report the presence of Nek2 throughout RA-induced differentiation and through overexpression studies and CRISPR-Cas9 ablation, demonstrate an essential role of Nek2 in neuron and astrocyte differentiation. ...

... SYP is a presynaptic marker that is specific for functionally mature neurons and is involved in synapse formation 22 . If these messages are reduced or removed, the nerve cells will die [25][26][27] . Recently, it has been found that the expression of SYP in nerve cells indicates the presence of functional synapses and the ability to generate action potentials 28,29 . ...

... It was also found that p107-mediated regulation of neural precursor number occurs through repression of Hes1 transcription, a downstream mediator of the Notch-signaling pathway, and strikingly, p107 deficiency led to a decreased number of matures neurons, as demonstrated by results of immunohistochemistry studies with NeuN, a marker for mature CNS neurons, and a reduction in the overall size/thickness of the cortex. It was later suggested that this decrease is not caused by increased cell death of committed neurons, but by apoptosis elevated in uncommitted progenitor cells, which is in accordance with previous work [55]. Moreover, short-and long-term BrdUlabeling studies revealed a striking defect in the rate at which p107 (−/−) progenitors commit to a neuronal fate, indicating that p107 regulates the transition from proliferating neural progenitor cells to committed neuroblast [56]. ...

... We therefore wanted to extend this study to the region of E1A encoded by the first exon outside of the well-studied CR3. We have utilized a series of N-terminus E1A deletions, the so-called Bayley mutants generated in the lab of Stan Bayley in the late 1980s [15,[22][23][24][25][26][27], to investigate how short deletions of E1A affect viral fitness. Firstly, we set out to determine how growth of these mutants is affected in comparison to the wt E1A-expressing mutant dl309 [14] in primary and contact-inhibited human lung fibroblasts WI-38 [28]. ...

... In this study, we aimed to find compounds of natural origin that effectively activate cardiogenesis through a well-defined mechanism. For this purpose, we developed an efficient cardiomyocyte-specific readout reporter system based on the mouse embryonic carcinoma cell line P19, which has a pluripotent nature capable of differentiating into three germ layers [22][23][24][25]. In this reporter system, P19 cells express mCherry fluorescent protein driven by the a-MHC (myosin heavy chain) promoter, which is activated upon cardiac induction. ...