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that contains a mutation in trans to the deletion allele will give an indication of the
severity of the mutation. If the phenotype of the unknown mutation is unchanged it is
considered to lack gene product (amorph), if more severe, it is considered to have
reduced gene product (hypomorph); if less severe, to be an overproducer (hyper-
morph) or to have taken on a new function (neomorph), which may not be detectable
over a deletion ( Muller, 1918 ).
A clever extension of this type of approach has been to use deletions for screening
of genetic loci whose zygotic expression is required for formation of specific tissue
types ( Ahnn and Fire, 1994; Chanal and Labouesse, 1997; Labouesse, 1997;
Te r ns et al., 1997 ). In one study, 77 genetic deficiencies covering an estimated
72% of the genome were screened for staining with antibodies to body wall
myosin ( Ahnn and Fire, 1994 ) and in another 90 deficiencies covering up to
75% of the genome were screened for loci affecting hypodermal development
( Chanal and Labouesse, 1997 ).
4. Deletions as Balancers
Deletions that suppress crossing over ( Broverman and Meneely, 1994; Jones et al.,
2009; Rosenbluth et al., 1990 ) are potentially useful as balancers ( Fig. 5 ). Mutations
close to the deletion that fall within the suppressed region can be effectively balanced
though rare recombination events can occur. As such deletions should only be used
when a more stable alternative is not available and balanced mutations should be
monitored regularly.
Fig. 5 Balancing a mutation using a deficiency. In this example, a deficiency is placed heterozygously
over a mutation that is outside the deletion but within the recombination suppressed region (dashed gray line).
Progeny from these animals will display either the deficiency phenotype (one quarter), the mut-x phenotype
(one quarter), or be WT in appearance (one half). Because mut-x is unlikely to recombine with the deficiency
chromosome the heterozygous strain can be maintained by selecting the WT progeny. If recombination does
occur, the breakdown of the strain can be observed by the loss of the mut-x phenotype in the progeny.
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