Human Chromosomes by Orlando J. Miller

By Orlando J. Miller

From the reports of the 3rd variation
"Each note "tells" during this concise gem of a human cytogenetics text...Superb association makes this a good text...for any cytogenetics course."
- American magazine of Human Genetics"

...the major textbook in English on human cytogenetics."
- Cell

Show description

By Orlando J. Miller

From the reports of the 3rd variation
"Each note "tells" during this concise gem of a human cytogenetics text...Superb association makes this a good text...for any cytogenetics course."
- American magazine of Human Genetics"

...the major textbook in English on human cytogenetics."
- Cell

Show description

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Extra info for Human Chromosomes

Sample text

Normal female karyotype by G-banding . , 1970) can be determined by cytophotometry; automated scanning methods facilitate such measurements. However, for many purposes flow cytometry has replaced cytophotometry. The flow cytometer is an instrument that can be used to measure the DNA content of single chromosomes at a rate of several thousand per minute. The flow cytometer converts a suspension of chromosomes that have 48 Centromeres and Kinetochores been doubly stained with two fluorochromes into microdrops and shoots these through a detector that measures the intensity of fluorescence of each microdrop at two wavelengths and prepares a statistical profile of all the measurements.

See text for further explanation (Ionsson and Hubscher, 1997, BioEssays, Vol. ). ) ( ( ORI ORI /S'~-'" 5' S ~ 5:. ~.. ··_3'.. 3 . Diagram showing synchronous replication in two adjacent units of replication (replicons), DNA synthesis begins at an origin (O RI) and proceeds in both directions, always 5' to 3' . Synthesis is continuous along the leading strand and discontinuous (occurring in Okazaki fragments) along the trail ing strand. Adjacent replication bubbles coalesce to yield two identical double helices of DNA.

2. I) . Cells arrest in G I and G2 if their DNA has been damaged (by ionizing radiation, say), and progression is delayed until DNA repair has occurred or celI death ensues. DNA damage triggers the sequential activation of proteins (Fig. , 1992), then the p53 tumor suppressor protein, and then the GADD45 protein, which binds to the proliferating cell nuclear antigen (PCNA) and blocks DNA replication (Chapter 3; Levine, 1997). There is also a spindle assembly checkpoint (Fig. 2. I) . CelIs arrest in G2 and delay their exit from mitosis in response to spindle microtubule disruption by spindle poisons such as colchicine, nocodazole, or benzimidazole.

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