Light-entrainment is a key property of circadian clocks, which relies on the induction of clock gene and protein expression. Light-induced expression in Per genes and/or proteins has been reported in vertebrate retinas. Together with the arrhythmic expression of most clock proteins, the absence of light-sensitivity of clock protein expression in the dopaminergic cells would argue against the presence of a functional circadian clock in these cells. In addition, to date no circadian phenotype has been linked to the clock mechanism within the dopaminergic cells, as the circadian rhythm in dopamine release requires the presence of a melatonin rhythm. Thus, while confirming the expression of circadian clock Lomitapide Mesylate components in dopaminergic cells, our data expose differences in the clock mechanism between cones and dopaminergic cells and question the cell autonomy of the later. However, dopaminergic amacrine cells could play a key role in the temporal organization of retinal function through the release of dopamine. Dopamine release is under the dual control of a circadian clock and light, with a peak during the day under light-adapted conditions and a trough at night in the dark, and is known to synchronize retinal rhythms, including in mammals. Thus, whether retinal dopamine neurons are autonomous circadian clocks remains an open question, but these cells may play a greater role in participating in the light entrainment of retinal rhythms and synchronization among retinal neurons rather than in initiating retinal pacemaker activity. In a way, retinal dopaminergic neurons may play a role similar to the retinocepient vasointestinal neuropeptidergic neurons of the SCN. Our observations in the retina may represent the case of more general organization of circadian clock cells that also occur in other tissues. For instance, emerging views for the organization of SCN rhythmic function emphasizes the strong heterogeneity in the individual properties of its cell-autonomous circadian oscillators and the important role of neuronal Mepiroxol networks in shaping a robust and coherent rhythmic output. However, although most SCN neurons express the core clock components, a link between specific SCN neuronal subtypes and rhythmic properties has been difficult to establish, and the means through which networks synchronize cellular oscillators and rhythmic outputs are still unclear. By demonstrating that clock components are widely expressed among retinal neurons and that a high degree of heterogeneity in their expression occurs among retinal cell types, our results suggest that the organization of populations of clock cells in retinal tissue may share similar features with that of the SCN. Dissecting the clock mechanism on a cell-type basis in the retina will thus likely shed light not only on the circadian organization of retinal function but also on the general organization of circadian clocks in mammalian tissues. Frameshift mutations within microsatellite sequences are caused by DNA polymerase slippage followed by a dysfunction of the mismatch repair system. A certain phenotype of MSI named EMAST has been observed in non-small cell lung, skin, ovarian, urinary tract, prostate, bladder, and recently colorectal cancer. However, the molecular basis for EMAST is incompletely understood. There is evidence for a rare association of EMAST with mutations in MLH1 and MSH2 in endometrial cancer. EMAST is commonly found in sporadic CRC and an overlapping mechanism may exist between MSI-low, EMAST, and loss of heterozygosity.