Biology Reference
In-Depth Information
developmental events. In the section below, which we shall briefly discuss
examples of how various factors may influence the timing of development.
2. EVIDENCE FOR MECHANISMS CONTROLLING THE
TIMING OF DEVELOPMENTAL EVENTS
Indirect evidence that developmental events are temporally controlled
comes from a plethora of evolutionary studies showing that heterochrony
constitutes an important evolutionary mechanism. Heterochrony ascribes
morphological differences between (usually closely) related clades to relative
changes in developmental timing, causing—for instance—acceleration or
retardation of organ growth, or the retention of juvenile features into adult-
hood (
Gould, 1977
). While evolutionary changes caused by heterochronic
constraints are obviously fixed genetically, they still illustrate the plasticity of
certain developmental traits, giving rise to the idea that gene programs
underlying these traits are easily adaptable not because these programs are
altered per se, but rather because their temporal appearance or duration
are “fine-tuned.”
More direct evidence for developmental timing comes from a large body
of genetic studies. If temporal regulators of development do exist, one would
hypothesize the existence of “temporal” mutations that affect primarily the
timing of certain development events, but leave the nature of the event itself
largely unaffected. The early 1980s saw the first examples of such “temporal”
mutations in the form of the “lineage” (lin) genes that were linked to
corresponding heterochronic mutations in
Caenorhabditis elegans
. Specifi-
cally, loss-of-function mutations of the
lin-14
and
lin-28
genes caused ani-
mals to skip certain cell fates, resulting in the precocious expression of
developmental events. In contrast, loss-of-function mutations in the
lin-
29
gene caused animals to re-iterate specific cell fates at later developmental
stages, instead of just during a single larval stage, and larval cell lineages con-
tinued to be active during the adult stage (
Ambros, 2003; Ambros &
Horvitz, 1984; Lee, Feinbaum, & Ambros, 1993
).
In other organisms, however, mutants with such well-defined temporal
defects are either remarkably scarce or simply not recognized as such. Given
that many “temporal” mutations would presumably wreak havoc in a devel-
oping organism, it stands to reason that most mutations that fall into this
category go unrecognized as such. However, some exceptions exist. In
humans, for instance, it has been argued that many morphological traits asso-
ciated with Down syndrome are heterochronic in nature. For instance,
