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To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.cell.2007.10.048 Byline: Deborah L. Berry (1)(2), Eric H. Baehrecke (1)(3) Keywords: CELLBIO; DEVBIO; SIGNALING Abstract: Autophagy is a catabolic process that is negatively regulated by growth and has been implicated in cell death. We find that autophagy is induced following growth arrest and precedes developmental autophagic cell death of Drosophila salivary glands. Maintaining growth by expression of either activated Ras or positive regulators of the class I phosphoinositide 3-kinase (PI3K) pathway inhibits autophagy and blocks salivary gland cell degradation. Developmental degradation of salivary glands is also inhibited in autophagy gene (atg) mutants. Caspases are active in PI3K-expressing and atg mutant salivary glands, and combined inhibition of both autophagy and caspases increases suppression of gland degradation. Further, induction of autophagy is sufficient to induce premature cell death in a caspase-independent manner. Our results provide in vivo evidence that growth arrest, autophagy, and atg genes are required for physiological autophagic cell death and that multiple degradation pathways cooperate in the efficient clearance of cells during development. Author Affiliation: (1) Center for Biosystems Research, University of Maryland Biotechnology Institute, College Park, MD 20742, USA (2) Present address: Children's National Medical Center, Washington, DC 20010, USA (3) Department of Cancer Biology, University of Massachusetts Medical School, Worcester, MA 01605, USA Article History: Received 12 June 2007; Revised 7 September 2007; Accepted 16 October 2007 Article Note: (miscellaneous) Published: December 13, 2007

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.cell.2005.07.026 Byline: Tamara Mikeladze-Dvali (1), Mathias F. Wernet (1), Daniela Pistillo (1), Esteban O. Mazzoni (1), Aurelio A. Teleman (2), Ya-Wen Chen (2), Stephen Cohen (2), Claude Desplan (1) Abstract: Color vision in Drosophila relies on the comparison between two color-sensitive photoreceptors, R7 and R8. Two types of ommatidia in which R7 and R8 contain different rhodopsins are distributed stochastically in the retina and appear to discriminate short (p-subset) or long wavelengths (y-subset). The choice between p and y fates is made in R7, which then instructs R8 to follow the corresponding fate, thus leading to a tight coupling between rhodopsins expressed in R7 and R8. Here, we show that warts, encoding large tumor suppressor (Lats) and melted encoding a PH-domain protein, play opposite roles in defining the yR8 or pR8 fates. By interacting antagonistically at the transcriptional level, they form a bistable loop that insures a robust commitment of R8 to a single fate, without allowing ambiguity. This represents an unexpected postmitotic role for genes controlling cell proliferation (warts and its partner hippo and salvador) and cell growth (melted). Author Affiliation: (1) Department of Biology, Center for Developmental Genetics, New York University, New York, New York 10003 (2) Developmental Biology Unit, European Molecular Biology Laboratory, Heidelberg, Germany Article History: Received 3 March 2005; Revised 7 June 2005; Accepted 25 July 2005 Article Note: (miscellaneous) Published: September 8, 2005

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.cell.2005.03.030 Byline: Kirst King-Jones (1), Jean-Philippe Charles (2), Geanette Lam (1), Carl S. Thummel (1) Abstract: A critical determinant of insect body size is the time at which the larva stops feeding and initiates wandering in preparation for metamorphosis. No genes have been identified that regulate growth by contributing to this key developmental decision to terminate feeding. We show here that mutations in the DHR4 orphan nuclear receptor result in larvae that precociously leave the food to form premature prepupae, resulting in abbreviated larval development that translates directly into smaller and lighter animals. In addition, we show that DHR4 plays a central role in the genetic cascades triggered by the steroid hormone ecdysone at the onset of metamorphosis, acting as both a repressor of the early ecdysone-induced regulatory genes and an inducer of the [beta]FTZ-F1 midprepupal competence factor. We propose that DHR4 coordinates growth and maturation in Drosophila by mediating endocrine responses to the attainment of critical weight during larval development. Author Affiliation: (1) Howard Hughes Medical Institute, Department of Human Genetics, University of Utah School of Medicine, 15 N 2030 E Room 5100, Salt Lake City, Utah 84112 (2) Universite de Bourgogne, UMR CNRS 5548, Developpement/Communication Chimique, Faculte des Sciences Gabriel, 6, Bd Gabriel, 21000 Dijon, France Article History: Received 27 September 2004; Revised 11 February 2005; Accepted 29 March 2005 Article Note: (miscellaneous) Published: June 2, 2005

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/S0092-8674(00)80679-0 Byline: David A Prober (1), Bruce A Edgar (1) Abstract: The Ras GTPase links extracellular mitogens to intracellular mechanisms that control cell proliferation. To understand how Ras regulates proliferation in vivo, we activated or inactivated Ras in cell clones in the developing Drosophila wing. Cells lacking Ras were smaller, had reduced growth rates, accumulated in G1, and underwent apoptosis due to cell competition. Conversely, activation of Ras increased cell size and growth rates and promoted G1/S transitions. Ras upregulated the growth driver dMyc, and both Ras and dMyc increased levels of cyclin E posttranscriptionally. We propose that Ras primarily promotes growth and that growth is coupled to G1/S progression via cyclin E. Interestingly, upregulation of growth by Ras did not deregulate G2/M progression or a developmentally regulated cell cycle exit. Author Affiliation: (1) Molecular and Cellular Biology Program, and Program in Developmental Biology, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, University of Washington, Seattle, Washington 98195, USA Article History: Received 4 August 1999; Revised 11 January 2000

Three proteins, namely, Hedgehog (Hh), Wingless (Wg) and Decapentaplegic (Dpp), are responsible for the growth and patterning of the Drosophila leg. Hh, which is secreted in the posterior cells, induces the dorsal anterior cells to secrete Dpp and the ventral anterior cells to secrete Wg. The complementary patterns of dpp and wg expression are studied. Results indicate that the patterns are maintained by mutual repression, which is essential for normal axial patterning.

The bithorax complex (BX-C) and the Antennapedia complex (ANT-C) are the primary hoemotic genes that specify body pattern in Drosophila and determine the genetic state of cells. The diversity of body patterns is related to the activities of ANT-C and BX-C, either alone or in combination. Homeobox genes such as the en, hh and dpp genes produce distinct boundaries in the wing to form compartments of cells of different patterns and polarities.

Research shows that organismal growth in Drosophila is initiated by the fat body possessing endocrine and storage functions of the vertebrate liver. Data indicate that the fat body functions as a nutrient sensor and contains slimfast gene whose downregulation leads to a global growth defect similar to that exhibited by Drosophila raised under poor nutritional conditions.

A localization mechanism for pair-rule transcripts was discussed which utilizes a new mRNP injection assay. It was shown that synthetic, fluorescently tagged fushi tarazu transcripts' ability to localize is impaired after its injection into blastoderm embryos. On the other hand, it was observed that rapid and specific apical localization that is dependent on an intact microtubule cytoskeleton occurs with nuclear protein extracts preincubation.