New York Area Drosophila Discussion Group

Abstracts

Rap1/Canoe Signaling Controls Diverse Aspects of Adherens Junctional Homeostasis and Epithelial Cohesion in Proliferating Tissues

Benjamin Bottner, Cold Spring Harbor Laboratory

The modeling of tissues relies on context-dependent segregation and cohesion of defined cell populations. In epithelia, E-cadherin levels and activity are vital for such sorting processes; however, the functional interplay of factors impinging on E-cadherin to modulate specific cell sorting events remains largely elusive. We demonstrate that the functions of Rap1 and Echinoid (Ed), two factors that affect adherens junction (AJ) formation and cell sorting behavior, are coordinated by Canoe (Cno). cno acts as a Rap1 effector in maintaining the circumferentially seamless distribution of AJs and the clonal cohesion exhibited by mitotic lineages. Over-expression of Cno triggers the accumulation of AJ proteins, and signals through Ed to expand adherens junctional perimeters. We provide further evidence that Cno in addition synergizes in parallel pathways with Crb and a Rap1- and Cno-independent activity of Ed in the general homeostasis of AJs. These observations define Cno as a critical mediator between pathways regulating AJ integrity and clonal cohesion.

Mechanical Regulation of Cytoskeletal Dynamics during Cell Intercalation

Rodrigo Fernandez-Gonzalez, Sloan Kettering Institute

Axis elongation in Drosophila embryos occurs through coordinated cell rearrangements driven by the activity of the cytoskeletal proteins actin and myosin II, which generate contractile forces. Using dual-color time-lapse imaging of living Drosophila embryos, we have found that actin and myosin II localize to two different pools in intercalating cells, one associated with cell-cell junctions and another located at the medial-apical cortex in a fibrous meshwork. We have used custom image analysis to show that junctional myosin forms multicellular cable-like structures that are actively assembled and contract to form rosettes, promoting efficient tissue elongation. Our results show that mechanical tension generated by actomyosin contractility inhibits myosin dissociation from cell-cell junctions, leading to myosin accumulation, cable assembly and contraction. Simultaneously, intercalating cells undergo cell shape fluctuations, with rapid cycles of apical expansion and contraction. Apical contraction is preceded by the assembly of highly dynamic, medial actomyosin structures, while disassembly of medial contractile structures precedes cycles of cell expansion. Intercalating cells also undergo cell shape fluctuations in mutant embryos where the adjacent mesoderm is not specified. Together, these results suggest that the dynamic assembly of medial actomyosin structures generates intrinsic forces that drive oscillatory behaviors in intercalating cells. Oscillatory behaviors may be necessary to accommodate the increasing cellular strain resulting from junctional contractility and axis elongation.

When Two Plus Two Doesn't Equal Four: Modeling Non-Additive Enhancer Behavior in the Drosophila melanogaster eve Promoter

Ah-Ram Kim, SUNY Stonybrook

The prediction of expression patterns from genomic sequence is a major research challenge in modern molecular genetics. Its solution requires an understanding of the transcriptional consequences for particular configurations of bound factors. One of the most informative experimental materials for such studies is an instance where the usual additive, modular behavior of enhancers breaks down. Such instances can reveal underlying rules, but the complexity of the experimental phenomena requires precise quantitative models for their interpretation. We developed a generalized and predictive model of quantitative, time-resolved mRNA expression of the Drosophila melanogaster gene even skipped (eve). I have used this model to understand non-additive behavior of 4 enhancer fusions of the -3.8 to -3.3 kb (stripe 3 enhancer) and the -1.6 to -1.1 kb (stripe 2 enhancer) regions of gene eve with and without spacer sequence between them. Quantitative gene expression data obtained by utilizing a site-specific RMCE technique allows for a precise computational analysis of gene expressions of multiple reporter constructs at single nuclei-6min temporal resolution. Analysis of non-classical behavior of 4 enhancer fusions revealed detailed biology of fundamental transcriptional mechanisms – competitive binding, cooperative binding, co-activation, direct repression and short-range quenching that are essential in the regulation of gene expression of eve. Furthermore, my computational model of eve is able to predict gene expressions of a variety of enhancers including stripe 2 elements of eve from 19 different Drosophila and Sepsis species and some of other pair-rule and gap gene enhancers with high accuracy.

Multiple Roles for Notch Signaling in Drosophila R7 Photoreceptor Specification

Andrew Tomlinson, Columbia University

Receptor tyrosine kinases (RTKs) and Notch proteins are different types of transmembrane receptors that transduce extracellular signals that control cell fate. Here we examine cell fate specification in the Drosophila ommatidium and examine how Notch acts together with the RTKs Sevenlesss (Sev) and the EGF receptor (DER) to define the R7 photoreceptor. The developing ommatidium grows by recruiting surrounding undifferentiated cells and then directing them to specific fates. The R7 photoreceptor derives from a cohort of three cells that are incorporated together. Two of these are specified as the R1/6 photoreceptor type by DER activation. These cells then activate N in the third cell (the R7 precursor), and this N signaling performs three roles. First it provides a block to photoreceptor specification; a block that DER signaling cannot overcome. The second role is (paradoxically) to negate the first; Notch signaling induces the expression of Sev which provides an RTK signal sufficient to overcome the block and thereby specify the cell as a photoreceptor. The third role is to designate the cell as the R7 type rather than the R1/6 photoreceptor type. We speculate why Notch activation has dual and opposite effects on photoreceptor differentiation within the prospective R7 cell, and provide a model for how Notch and RTK signaling combine to specify the distinct fates of the R1/6 and R7 photoreceptors as well as the surrounding non-neuronal cone cells.

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