, 1998). MAPK is a complex signal transduction pathway that

promotes cell division and can also be mediated through the binding of extracellular growth factors (e.g. FGF-2 and EGF) to cell surface receptors (Fgfr2 and Egfr). Both FGF2 and EGF have been previously implicated to regulate adult neurogenesis in vivo (Frinchi et al., 2008; Mudòet al., 2009; Doetsch et al., 2002; Basak & Taylor, 2009). Disregulation of Galr2 has been linked to depression in human and mouse (Lu et al., 2007). There are currently six unknown SNPs that exist between A/J and C57BL/6J. Two are in the 5′ untranslated region, check details three are in intron-1, and one is in the 3′ untranslated region. Septin 9 (Sept9) and cyclin-dependent kinase 3 (cdk3) are two other genes that are worth mentioning because even though they are not directly linked to neurogenesis, they are both cell cycle regulatory genes. Sept9 is involved in the progression through G1 of the cell cycle and it is

highly expressed throughout the adult mouse brain (Gonzalez et al., 2009). By contrast, cdk3 is expressed at low levels throughout the adult mouse brain and it is required for G1–S transition (Braun et al., 1998). The Sept9 gene is the largest (∼162 kb) gene identified in the QTL interval and it harbors 127 SNPs with unknown functions. By contrast, the cdk3 gene is shorter in length (∼4.3 kb) and contains only eight functionally unknown SNPs. The RMS is a major source of new neurons in the adult brain. Despite the intensive analysis Acalabrutinib of the cytoarchitecture of the RMS, the molecular genetic

mechanisms regulating the size and behavior of the RMS proliferating population remain elusive. In this study, we investigated the genetic contribution of the natural variation selleck compound observed in RMS proliferation. By using BrdU immunohistrochemistry and stereological methods, we have demonstrated that the numbers of proliferating cells in the RMS are highly variable among C57BL/6J, A/J and their RI strains, and based on QTL mapping, this phenotypic variation is generated in part by the allelic differences at a locus on Chr 11. In this study, we discovered that the proliferative capacity of the adult RMS behaves as a quantitative trait where the numbers of rapidly proliferating cells in the RMS varies 1.7-fold between the parental strains (C57BL/6J and A/J) and 3.6-fold among the AXB/BXA RI strains. We found that these differences are not due to the strain differences in S-phase lengths based upon our analysis of the cell cycle. This is the first characterization of the proliferative behavior of dividing precursors in the mouse RMS in terms of cell cycle kinetics. Our cell cycle analysis did not detect any significant differences in either cell cycle or S-phase lengths between A/J and C57BL/6J, suggesting that it is the differences in the number of proliferating RMS cells that account for the strain differences.