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EdU labeling uses a modified nucleoside, 5-ethynyl-2'-deoxyuridine, incorporated into newly synthesized DNA, then chemically couples it to a fluorescent reporter.

A 2008 experiment injected adult mice with $100\mu \mathrm{g}$ of this label and inspected intestinal sections 96 hours later. Fixed sections on slides received $10\mu \mathrm{M}$ Alexa568-azide for 10 minutes. Imaging with a fluorescence microscope combined the reporter image with a Hoechst DNA counterstain and a transmitted-light view. Labeled cell nuclei marked descendants of biological cells synthesizing DNA during exposure, rather than identifying current S phase at collection. ^[ref]

The same study's cultured-cell controls compared overnight $10\mu \mathrm{M}$ label, no label, and label with $10\mathrm{mM}$ hydroxyurea. No-label samples had little reporter background; hydroxyurea strongly suppressed incorporation. The camera detected residual signal with a 3-second exposure versus 40 milliseconds under otherwise identical settings, demonstrating why acquisition settings matter. These controls support synthesis-dependent labeling, without proving that every labeled biological cell completes division. ^[ref]

A nucleoside comprising guanine attached to ribose. Its free $3^{\prime }$ hydroxyl group initiates group I intron RNA splicing; guanosine is incorporated into the excised intron, rather than acting as a regenerated catalyst.

A nucleoside combines a nucleobase with a sugar, without the phosphate groups of a nucleotide. Adenosine is the nucleoside built from adenine and ribose. See Alberts et al., Molecular Biology of the Cell: nucleosides and nucleotides.

Base composition changes both the initial buoyant density and the size of the BUdR-induced density increment. The fraction-number axis runs toward lower density. The unlabelled viral peak lies at a lower fraction number than the corresponding host peak, consistent with viral DNA having a higher GC content. BUdR replaces thymidine in newly synthesized strands, so relatively AT-rich DNA incorporates more brominated nucleoside per unit length and undergoes a larger density increase.

Consequently the more AT-rich host DNA can overtake the viral DNA in the fully substituted class: the host fully heavy peak is slightly farther toward the dense end, although host unlabelled DNA was less dense. The hybrid peaks are intermediate. A useful qualitative model is ${\rho }_{LL}={\rho }_0(g)$, ${\rho }_{LH}={\rho }_0(g)+\Delta \rho (g)/2$ and ${\rho }_{HH}={\rho }_0(g)+\Delta \rho (g)$, where $g$ is GC fraction, ${\rho }_0$ increases with $g$, and $\Delta \rho$ decreases as the thymidine fraction decreases. Unequal substitution efficiencies could contribute, but different replication mechanisms are unnecessary. These are equilibrium density positions, not molecular-length measurements.