DOI
10.5642/aliso.19911301.08
First Page
191
Last Page
206
Abstract
Parallelism as one of the forms of biological similarity is investigated in the light of recent findings from developmental and molecular biology. From the organismic point of view, functional constraints and evolutionary canalization are well established as causes of parallelism. To these may be added, from the molecular perspective, (a) erratic activations of repressed genes; (b) activations of alternative pathways under the influence ofhomoeotic genes; and (c) horizontal gene transfer, for which a simple mechanism is proposed. The control of gene expression through the action oftransposable elements, reversible to some degree, appears to be an evolutionarily important and frequent phenomenon, which may account for many cases formerly interpreted as losses or irreversible changes of genes. It is suggested that this mechanism, which seems to be optimized in angiosperms, may account for the great evolutionary plasticity of this plant group. It may also provide an explanation for so-called reversals which appear as artifacts of character analyses and are biologically barely explicable. Events of horizontal gene transfer, creative for evolution but disturbing for classification, appear less frequent, or otherwise the structure of the taxonomic hierarchy would not be perceptible. Increasing knowledge in the fields of molecular and developmental biology tends to blur the borderline between homology, homoiology, parallelism, and perhaps convergence, phenomena formerly thought to be more or less distinct.
Recommended Citation
Kubitzki, K.; von Sengbusch, P.; and Poppendieck, H.
(1991)
"Parallelism, It's Evolutionary Origin and Systematic Significance,"
Aliso: A Journal of Systematic and Floristic Botany:
Vol. 13:
Iss.
1, Article 8.
Available at:
https://scholarship.claremont.edu/aliso/vol13/iss1/8
Rights Information
© 1991 K. Kubitzki, P. V. Sengbusch, H. Poppendieck
Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 License.