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ShareSep. 27, 2005 — A pair of research papers published this week report findings that increase our understanding of how an organism's body size is determined and how the speed of its development is controlled. In particular, the work sheds light on the molecular and cellular pathways that act to convey information about a growing organism's size, as well as on pathways that use that information to correctly time critical transitional events during development.
The two studies are reported in Current Biology online on September 22 by Dr. Philip E. Caldwell and colleagues of Rice University and Dr. Christen Mirth and colleagues of the University of Washington.
Previous work had shown that there is a close linkage between the final body size of an organism and the length of its developmental stages: Elephants are larger and develop more slowly than mice. However, the mechanisms by which body size and developmental rate are controlled remain incompletely understood.
Both studies examine the control of larval development in the fruit fly Drosophila. Fruit flies undergo three successive larval stages and molts before undergoing metaphorphosis and emerging as adult flies. In insects, it was previously found that the release of the hormone ecdysone from an endocrine organ called the prothoracic gland triggers larval molting and, ultimately, metamorphosis. Thus, researchers have speculated that the timing of ecdysone release is critical in determining both the final body size and developmental rate of an insect.
In their new work, Philip Caldwell, Magdalena Walkiewicz, and Michael Stern manipulated the timing and amount of ecdysone release during development of the fruit fly. They induced precocious ecdysone release by specifically expressing an activated form of the signaling molecule Ras in the endocrine prothoracic gland. This precocious ecdysone release caused flies to develop more rapidly and exhibit a much smaller body size than normal. In contrast, inhibiting Ras in the prothoracic gland prevented ecdysone release and delayed development, creating flies that are much larger than normal. On the basis of their findings, the investigators conclude that Ras activity in the prothoracic gland regulates body size and developmental rate by regulating ecdysone release.
In the second study, Christen Mirth, James W. Truman, and Lynn M. Riddiford address how developing flies sense that they have reached the proper size to initiate a new phase of development. Their new findings show that the prothoracic gland'the organ that releases ecdysone'itself acts as a size-sensing tissue. The researchers found that by manipulating the growth of specific cells within the gland, they were able to control the timing of metamorphosis and the body size of adult flies. They showed that artificial enlargement of the prothoracic gland appeared to cause an overestimation of the larval flies' overall body size, prompting the initiation of metamorphosis before the flies surpassed the minimal viable weight necessary to survive pupation. On the basis of their findings, the authors propose that under normal conditions, growth of prothoracic gland during development helps larval flies determine when a critical body weight has been reached and when metamorphosis should be initiated.
Mirth et al.: 'The Role of the Prothoracic Gland in Determining Critical Weight for Metamorphosis in Drosophila melanogaster.' Publishing in Current Biology online on September 22, 2005. DOI 10.1016/j.cub.2005.09.017 www.current-biology.com.
Caldwell et al.: 'Ras Activity in the Drosophila Prothoracic Gland Regulates Body Size and Developmental Rate via Ecdysone Release.' Publishing in Current Biology online on September 22, 2005. DOI 10.1016/j.cub.2005.09.011 www.current-biology.com.
The researchers include Christen Mirth, James W. Truman, and Lynn M. Riddiford of University of Washington in Seattle. This project was funded by the Royalty Research Fund and the Virginia and a Prentice Bloedel Professorship.
The researchers include Philip E. Caldwell, Magdalena Walkiewicz, and Michael Stern of Rice University in Houston. This work was supported by a National Institutes of Health grant.
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