Worm Breeder's Gazette 11(4): 74

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.

age-1 and fer-15 are Separate Genes

E.W. Hutchinson and T.E. Johnson

The fundamental mechanisms of reproduction and survival are being 
explored through the analysis of genetic stocks that have reduced 
fertility and postponed senescence.  age-1(hx546) is a recessive 
mutant allele that results in an average 40% increase in life span at 
20 C and an average 65% increase at 25 C.  Mutant males also show 
extended life spans.  Associated with the increased life span is a 75% 
decrease in hermaphrodite self-fertility (Friedman and Johnson, 
Genetics 118: 75-86, 1987).  The long-lived phenotype was not 
separable from fer-15(b26), a temperature-sensitive locus on linkage 
group II causing defective spermatogenesis.  It was not clear whether 
age-1 was a further mutation in fer-15 or just tightly linked to fer-
15.  We now have three separate lines of evidence to show (1) that age-
1 and fer-15 are distinct genetic loci and (2) that the decrease in 
self-fertility is due to fer-15, not age-1 as had previously been 
Multifactor Crosses: In recombinants selected between dpy-10 and unc-
4, the decreased self-fertility cosegregates with fer-15 but long life 
span does not.  We have therefore separated lines with (1) wild-type 
life span and wild-type self-fertility, (2) wild-type life span and 
decreased self-fertility, (3) long life span and decreased self-
fertility, and (4) long life span and wild-type self-fertility.
Deficiency Analysis: Using a series of deficiencies covering much of 
the region between dpy-10 and Unc-4, the decreased self-fertility 
phenotype was assigned to the same region as were fer-15 and emb-27.  
The long life span phenotype was not assigned to this same region, but 
rather to a region between let-23 and unc-4.  We are mapping age-1 
more precisely using a second set of deficiencies through this region. 
Tc1 Recombinants: A Bristol/Bergerac congenic was constructed in 
which the Bergerac wild-type alleles of fer-15 and age-1, together 
with several centiMorgans of flanking DNA containing many Tc1 elements,
have been introgressed into an otherwise Bristol (N2) genetic 
background.  Recombinants of this congenic crossed with a dpy-10 
age-1 ere chosen.  We 
then assayed their Tc1 patterns, temperature-sensitive defective 
spermatogenesis, self-fertility, and life span.  fer-15 and decreased 
self-fertility cosegregated and mapped to the middle of the region 
containing novel Tc1 bands.  Life span (age-1) mapped further to the 
right, closer to unc-4.  
These three lines of evidence provide a consistent interpretation of 
the relationship between fer-15 and age-1.  These are two separate, 
closely linked genes.  fer-15(b26) is responsible for both temperature-
sensitive defective spermatogenesis and decreased self-fertility.  age-
1(hx546) is responsible for long life span.  
We have identified the location of fer-15 on the physical map by 
deletion mapping (see Tedesco & Johnson).  The location of age-1 will 
be identified through the mapping of Tc1 and Non-Tc1 polymorphisms in 
the Tc1 recombinants described above.  The actual cloning of the genes 
will involve transformation of mutants with the wild-type alleles and 
sequence analysis to identify the mutational events responsible for 
the alteration of fertility and life span.