The Questions of Developmental Biology

Snapshot Summary: The Environmental Regulation of Development
1. The environment can affect development in several ways. Development is sometimes cued to normal
circumstances that the organism can expect to find in its environment. The larvae of many species will not
begin metamorphosis until they find a suitable substrate. In other instances, symbiotic relationships
between two or more species are necessary for the complete development of one or more of the species.
2. Developmental plasticity makes it possible for environmental circumstances to elicit different
phenotypes from the same genotype. Many species have a broad reaction norm, wherein the genotype can
respond in a graded way to environmental conditions.
3. Some species exhibit polyphenisms, in which distinctly different phenotypes are evoked by different
environmental cues.
4. Seasonal cues such as photoperiod, temperature, or type of food can alter development in ways that make
the organism more fit. Changes in temperature also are responsible for determining sex in several
organisms, including many types of reptiles and insects.
5. Predator-induced polyphenisms have evolved such that the prey species can respond morphologically to
the presence of a specific predator. In some instances, this induced adaptation can be transmitted to the
progeny of the prey.
6. The differentiation of immunocompetent cells and the formation of synapses in the visual system are
examples where experience influences the phenotype.
7. Compounds found in the environment (teratogens) can disrupt normal development. Teratogens can be
naturally occurring substances or synthetic ones.
8. Alcohol and retinoic acid are two of the most intensively studied human teratogens. They may produce
their teratogenic effects through more than one pathway.
9. It is possible that numerous compounds may be acting as hormone mimics or antagonists disrupt normal
development by interfering with the endocrine system.
10. Genetic differences can predispose individuals to being affected by teratogens.
*In some cases, the same condition can be caused by a disruption (from an exogenous agent) or a malformation (from
the nucleus). For instance, certain axial malformations in mice can be produced either by the administration of retinoic
acid or by mutations in certain Hox genes. In some instances, the mutation and the teratogen are known to affect the
same enzyme. Chondroplasia punctata is a congenital defect of bone and cartilage, characterized by abnormal bone
mineralization, underdevelopment of nasal cartilage, and shortened fingers. It is caused by a defective gene on the X
chromosome. An identical phenotype is produced by the ingestion of the rat-killing compound, warfarin. It appears that
the defective gene is normally responsible for producing an arylsulfatase protein necessary for cartilage growth. The
warfarin compound inhibits this same enzyme (Franco et al. 1995).
This is a critical public health concern, because there is significant overlap between the population using acne medicine
and the population of women of childbearing age, and because it is estimated that half of the pregnancies in America
are unplanned (Nulman et al. 1997). Vitamin A is itself teratogenic when injected in megadose amounts. Rothman and
colleagues (1995) found that pregnant women who took more than 10,000 international units of preformed vitamin A
per day (in the form of vitamin supplements) had about a 2 percent chance of having a baby born with disruptions
similar to those produced by retinoic acid.
For a sensitive account of raising a child with fetal alcohol syndrome, as well as an analysis of FAS in Native American
culture in the United States, read Michael Dorris's The Broken Cord 1989. The personal and sociological effects of
FAS are well integrated with the scientific and economic data