Worm Breeder's Gazette 11(4): 73

These abstracts should not be cited in bibliographies. Material contained herein should be treated as personal communication and should be cited as such only with the consent of the author.

Effects of Deficiencies on Hermaphrodite Fertility

Anne Brooks and Tom Johnson

We are interested in genes specifying life-history traits such as 
longevity, fertility, fecundity, and rate of development.  Currently, 
we are looking for genes in the C1-balanced region of LGII that 
decrease hermaphrodite fertility.  Since we hope to use deficiency 
stocks to map these genes, we have assayed the brood sizes of 
heterozygous deficiency stocks in order to establish the effects of 
deficiencies on fertility.
We anticipated at least two ways that deficiencies might affect the 
brood sizes: (1) A negative correlation between size of deficiency and 
fertility could exist.  This is based on a model where many genes 
would have additive effects on fertility, the classic assumption of 
quantitative genetics.  (2) Certain genes might be haplo-insufficient 
such that one copy fails to make enough gene product for wild-type 
fertility to be expressed.
We tested for a correlation between deficiency size and brood size 
using two different metrics of defining the deficiency size.  First, 
we simply correlated the size of the deficiency in map units with 
brood size.  We obtained a negative, but not significant correlation (-
.28, P = .13).  Second, we tried correlating the brood size with the 
number of known genes uncovered by each deficiency.  This correlation 
was also negative and not significant (-.17, P = .36).  Obviously, 
these results show no significant additive effects of deficiency size. 
In fact, the size of deficiency accounts for only 3 to 8% of the 
variance observed in brood size.
We tested for haplo-insufficiency through a simple deficiency 
analysis, i.e., we looked for regions which gave a consistently 
reduced brood size when uncovered by a deficiency.  We observed two 
regions that displayed a substantial decrease in fertility when 
uncovered by a deficiency.  Stocks containing deficiencies of the dpy-
10 to spe-1 region or the let-237 to let-238, 
onsistently yield brood sizes of less than 
150, while stocks containing deficiencies that border these regions 
produce broods of 150 and above.  Therefore, our results do show some 
evidence for haplo-insufficient sites.
In conclusion, our analysis of the effects of LGII deficiencies on 
brood size does not show any evidence of additivity based on number of 
genes removed.  We do detect haplo-insufficient regions where 
codominant fertility mutations might be found by mutation.  We will 
continue screening for low-brood mutants and plan to map these 
fertility mutations through deficiency mapping.