On the cover: In the late 1980s, the labs of Bob Horvitz, Victor
Ambros, and Gary Ruvkin were studying a C. elegans mutant that
had a developmental defect such that, as the animals matured,
they maintained several larval-stage cells and did not develop
many adult cells and structures. This mutant was said to be due
to a defect in lin-4, but at the time, they didn't know what
exactly lin-4 was. In 1987, Chip Ferguson in the Horvitz lab
identified a mutant with a mutation in lin-14 that suppressed
the effect of the lin-4 mutant. (Nature, 326, 259-267). This led
to the hypothesis that lin-4 negatively regulated lin-14, a
proposal that was supported by the fact that animals with null
mutations in lin-14 had a phenotype opposite to that of those
with the lin-4 mutation (Science, 226, 409-416). While Rosalind
Lee and Rhonda Feinbaum worked with Ambros to determine the
sequence of lin-4, Gary Ruvkin's lab identified conserved
sequence in the 3′ UTR of lin-14 that was involved in the
downregulation by lin-4. The shar