New York Area Drosophila Discussion Group

New York Area Drosophila Discussion Group meetings are held twice a year from 6-8 PM, followed by a reception. Each meeting includes four talks by graduate students and postdocs presenting new data from fly labs in the greater New York area.

Organizers: Mary Baylies, Sloan-Kettering Institute; Laura Johnston, Columbia University; Jennifer Zallen, Sloan-Kettering Institute

Speakers: Agata Becalska, Princeton University; Carlos Estella, Columbia University Medical Center; Hsiao-lan Liang, New York University; Aloma Rodrigues, NYU School of Medicine

Agenda

Zelda, A Key Regulator of the Maternal-to-zygotic Transition
Hsiao-lan Liang, New York University

Molecular Logic of Ventral Appendage Development
Carlos Estella, Columbia University Medical Center

Bazooka Mediates Cortical Exclusion of Posterior Determinants during Oogenesis
Agata Becalska, Princeton University

Stat92E and dMyc act in Parallel to Promote Cellular Growth by Regulating Ribosomal Biogenesis
Aloma Rodrigues, NYU School of Medicine

Abstracts

Molecular Logic of Ventral Appendage Development
Carlos Estella and Richard Mann, Columbia University Medical Center

Limb formation is a great model to study cell specification, tissue growth and cell differentiation during animal development. In many animal phyla the expression in embryos of the homeodomain containing gene Dll marks the field where the appendages will form. In Drosophila the precursors of the legs are specified during embryogenesis by the expression Dll. During larval stages Dll expression is transiently activated by two signalling pathways, the Dpp (TGfß) and Wg (Wnt) pathways until its expression is maintained by an unkown mechanism. Here we describe how Dll expression is controlled by a group of cis-regulatory elements that account for its expression during leg development. Moreover, the identification of these enhancers allow us to subdivide the leg primordia in three mutually exclusive domains with different fates: the coxopodite or the extension of the body wall, the telopodite that will give rise to the true appendage, and the progenitors of the Keilin Organs (KO), a larval sensory structure associated with the leg disc. Dll function is required for the last two fates, and its expression is regulated by two separate enhancers.

The "Leg Trigger" (LT) enhancer controls Dll expression in the telopodite precursors cells and the "DKO" ("Distalless Keilin Organ") enhancer drives Dll in the KO progenitor cells. Moreover we elucidate the signals that control the expression of all these enhancers and their spatial relationship. In the case of the LT enhancer we also show that this element integrates the Wg and Dpp inputs by directly binding the transcriptional effectors of these pathways. In addition, the LT enhancer synergizes with the Dll promoter to maintain its own expression after its initial activation by the Wg and Dpp signals, in part, by an autoregulatory mechanism. This two-component mechanism explains how dorsal and ventral Dpp and Wg gradients can be converted into stable domains of gene expression along the proximo-distal axis.

Bazooka Mediates Cortical Exclusion of Posterior Determinants in the Oocyte
Agata N Becalska and Elizabeth R Gavis, Princeton University

Patterning of the anterior-posterior (A-P) axis in Drosphila is governed by the localization of maternally derived determnants to the anterior and posterior poles of the developing oocyte. Factors localized to the posterior comprise the germ plasm, and are ultimately responsible for the formation of the germ line as well as the patterning of the A-P axis. While some basic mechanisms underlying localization of germ plasm components have been elucidated, the process by which these molecules are specifically targeted to the posterior and anchored exclusively at the posterior cortex is poorly understood.

The Par proteins Par-1 and Bazooka (Baz, Par-3) form mutually exclusive complexes in the oocyte, and are localized to the posterior and lateral cortex respectively. As these proteins are involved in setting up distinct cortical subdomains in other systems, they are attractive candidates for spatial restriction of the germ plasm within the oocyte. To address this question, we are investigating the effect of a hypomorphic allele of baz on germ plasm localization and A-P patterning. Here we present data suggesting that Bazooka plays a role in cortical exclusion of germ plasm components in the oocyte.

Stat92E and dMyc act in Parallel to Promote Cellular Growth by Regulating Ribosomal Biogenesis
Aloma Rodrigues and Erika Bach, NYU School of Medicine

Developing organisms achieve reproducible size by balancing proliferation, cellular growth and apoptosis. We previously reported that JAK/STAT signaling increases the total mass of the developing Drosophila eye. To define the requirement of the sole Drosophila STAT protein Stat92E in growth control, we induced stat92E clones at precise times in development and measured their size as compared to their sister wild type clones. In the eye and wing, stat92E clones are substantially smaller than their sister clones, but in a Minute background, they can obtain larger sizes. These data indicate that Stat92E is required for clone survival and that cells lacking it are eliminated by cell competition.

A central regulator of cellular growth and cell competition is dMyc, the sole Drosophila c-Myc homolog. Cells with higher levels of dMyc are super-competitors and grow at the expense of their (lower dMyc-expressing) neighbors. In contrast, cells with reduced dMyc (low-dMyc cells) are eliminated by surrounding wild type cells. We assessed whether hyper-activating Stat92E in low-dMyc cells would promote their survival. Indeed, low-dMyc cells with activated Stat92E are rescued from the effects of competition, a significant finding since only BMP pathway genes have been reported to rescue these cells. These experiments were performed in a background in which the endogenous dmyc gene was intact, raising the possibility that Stat92E promotes survival of low-dMyc cells by increasing dmyc levels. To address this possibility, we made low-dMyc clones with activated Stat92E but lacking the endogenous dmyc gene. We find that activated Stat92E can rescue low dMyc-cells even in the absence of the dmyc gene, suggesting that Stat92E and dMyc act in parallel to regulate cellular growth. Consistent with this model, we find that activation of Stat92E, like over-expression of dMyc, increases ribosomal biogenesis but does not alter mitochondrial activity. These results demonstrate for the first time that JAK/STAT signaling has a direct effect on ribosomal biogenesis and suggest that Stat92E and dMyc have common growth-regulatory target genes.