The formation of a colorless waxy c wx spot in a

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The formation of a colorless, waxy ( c - wx ) spot in a colorless, nonwaxy ( c - Wx ) patch is due to a second breakage event that eliminates the dominant A468 Chapter 20: Cancer C Wx C Wx C-Wx c-Wx (A) C gene has been lost Wx Wx BRIDGE–BREAKAGE– FUSION extra copies of C gene C-Wx C-C-Wx (C) C Wx C Wx C C C C Wx Wx BRIDGE–BREAKAGE– FUSION Wx Wx gene has been lost Wx (B) C-Wx c-Wx c-wx BRIDGE–BREAKAGE– FUSION Figure 20–17 Formation of three different types of patches observed in speckled kernels ( Answer 20–58 ). (A) Formation of a colorless, nonwaxy ( c-Wx ) spot. (B) Formation of a colorless, waxy ( c-wx ) spot inside a colorless, nonwaxy ( c-Wx ) spot formed as in (A). (C) Formation of an intensely colored, nonwaxy ( C-C-Wx ) spot. Vertical arrows pointing to the dicentric chromosomes show the positions of the breaks that lead to formation of the patches. In each case the upper half of the starting dicentric chromosome gives rise to the new dicentric chromosome.
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nonwaxy ( Wx ) allele (Figure 20–17B). In the absence of the dominant allele the spot is waxy ( wx ) due to the recessive allele on the normal chromosome (not shown). The formation of an intensely colored patch is due to a breakage event that leads to a dicentric chromosome with multiple copies of the dominant color allele (Figure 20–17C). Thus, the genetic constitution of the intensely colored patch is C - C - Wx . B. You would never expect to see a colored spot within a colorless patch because, once eliminated, the dominant color ( C ) allele cannot be regained by further bridge–breakage–fusion cycles. C. You would expect to see colorless spots within an intensely colored patch because the dominant color ( C ) allele could be lost by subsequent bridge–breakage–fusion cycles. The demonstration by McClintock of bridge–breakage–fusion cycles in plants was one of the earliest indications that the broken ends of chromo- somes are in some way ‘sticky’—entirely different from natural chromosome ends. It is clear now that cells have an active repair pathway for joining bro- ken DNA ends together as a defense against potentially lethal double-strand breaks. So long as breaks are rare, the correct ends are joined. But when mul- tiple breaks are present, the wrong partners can be joined, leading to translocations or other genetic rearrangements. In humans, such rearrange- ments are often associated with cancers. Reference: McClintock B (1939) The behavior of successive nuclear divi- sions of a chromosome broken at meiosis. Proc. Natl Acad. Sci. U.S.A. 25, 405–416. CANCER TREATMENT: PRESENT AND FUTURE DEFINITIONS 20–59 Gleevec 20–60 Multidrug resistance 20–61 Gene expression profile TRUE/FALSE 20–62 True. Useful therapies selectively target cancer cells and leave normal cells relatively unaffected. This selective action always depends on a key differ- ence between normal cells and cancer cells. For example, most anticancer drugs and ionizing radiation damage DNA. These treatments preferentially kill cancer cells because the cancer cells have a diminished capacity to sur- vive the damage.
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