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• W1993676881 abstract "Tissue and organ architectures are incredibly diverse, yet our knowledge of the morphogenetic behaviors that generate them is relatively limited. Recent studies have revealed unexpected mechanisms that drive axis elongation in the Drosophila egg, including an unconventional planar polarity signaling pathway, a distinctive type of morphogenetic movement termed “global tissue rotation,” a molecular corset-like role of extracellular matrix, and oscillating basal cellular contractions. We review here what is known about Drosophila egg elongation, compare it to other instances of morphogenesis, and highlight several issues of general developmental relevance. Tissue and organ architectures are incredibly diverse, yet our knowledge of the morphogenetic behaviors that generate them is relatively limited. Recent studies have revealed unexpected mechanisms that drive axis elongation in the Drosophila egg, including an unconventional planar polarity signaling pathway, a distinctive type of morphogenetic movement termed “global tissue rotation,” a molecular corset-like role of extracellular matrix, and oscillating basal cellular contractions. We review here what is known about Drosophila egg elongation, compare it to other instances of morphogenesis, and highlight several issues of general developmental relevance. The most captivating aspect of biology to the youngest budding scientist may be the diversity of animal forms. Darwin memorably expressed this sentiment as “endless forms most beautiful” (Darwin, 1859Darwin C. On the Origin of Species by Means of Natural Selection. Murray, London1859Google Scholar); both external bodies and their internal organ counterparts display wonderful, and wonderfully diverse, forms. These forms do not of course exist for our aesthetic appreciation; instead they adhere to the maxim “form follows function.” To give just one example, the function of many of our own organs, including vasculature, kidneys, and lungs, depends on the construction of a highly branched network of elongated tubules. In order to understand how organs and indeed organisms function, we need to understand the processes that generate such forms during development. The mechanisms that drive tissue and organ morphogenesis are subjects of long-standing interest. Embryonic events such as gastrulation and axis extension have been extensively studied, particularly in externally fertilizing animals such as sea urchins, sea squirts, frogs, fish, worms, and flies. Despite this diversity, research to date has uncovered a fairly limited but highly conserved repertoire of cell behaviors that mediate morphogenesis (Quintin et al., 2008Quintin S. Gally C. Labouesse M. Epithelial morphogenesis in embryos: asymmetries, motors and brakes.Trends Genet. 2008; 24: 221-230Abstract Full Text Full Text PDF PubMed Scopus (74) Google Scholar). For instance, apical constriction of epithelial sheets drives tissue invagination during gastrulation across many species, as well as subsequent developmental events (Sawyer et al., 2010Sawyer J.M. Harrell J.R. Shemer G. Sullivan-Brown J. Roh-Johnson M. Goldstein B. Apical constriction: a cell shape change that can drive morphogenesis.Dev. Biol. 2010; 341: 5-19Crossref PubMed Scopus (310) Google Scholar). Similarly, many species utilize convergent extension, in which a group of cells converge along a common midline and intercalate, to elongate the body axis (Keller, 2002Keller R. Shaping the vertebrate body plan by polarized embryonic cell movements.Science. 2002; 298: 1950-1954Crossref PubMed Scopus (566) Google Scholar). Yet while these are several examples of well-understood processes, our study of animal morphogenesis is really in its infancy. We need to know all the dynamic cellular behaviors that shape tissues, uncover the mechanisms by which these are individually and collectively regulated, and understand how these molecular mechanisms interface with cell and tissue mechanical properties to actually sculpt organs. This Perspective will discuss mechanisms that confer the simple oval shape of the Drosophila egg, a relatively unexamined process that is shedding new light on the above issues. Drosophila oogenesis has a long history of study, dating back to the pioneering descriptions of King (King, 1970King R. Ovarian Development in Drosophila melanogaster. Academic Press, New York1970Google Scholar, King et al., 1956King R.C. Rubinson A.C. Smith R.F. Oogenesis in adult Drosophila melanogaster.Growth. 1956; 20: 121-157PubMed Google Scholar), and has numerous features that render it attractive to developmental biologists (Spradling, 1993Spradling A. Developmental genetics of oogenesis.in: Bate M. Martinez-Arias A. The Development of Drosophila Melanogaster. CSHL Press, New York1993: 1-70Google Scholar). One advantage is the simplicity of the organ. Drosophila eggs arise from individual units called follicles (or egg chambers), which consist of just two cell types, the germline and a surrounding somatic epithelium (Figure 1C ). A germline cyst, which contains 15 supporting nurse cells and a single oocyte, forms the core of each follicle. The cyst is encased within a simple monolayered epithelium of “follicle cells” (FCs); FCs contact the germline at their apical surfaces while their basal surfaces lie along a basement membrane. A second advantage is the anatomical organization of the ovary (Figure 1A). The stem cell populations that generate the germline and somatic follicle components reside in the anterior of an ovariole; each follicle moves posteriorly as it develops and is separated from neighboring follicles by intervening stalk cells (Figure 1B). An ovariole contains six to eight follicles of increasing maturity, vividly illustrating why it can be called an “egg assembly line,” and providing snapshots of the ∼7.5 days of development between the initial stem cell division and the mature egg. A third advantage is that the rich biology of oogenesis can be investigated with the full power of Drosophila genetics, via both classical female sterile approaches and more contemporary genetic mosaic analyses. These features have made Drosophila oogenesis an important system for the study of diverse biological processes, from DNA replication to pattern formation to stem cell and miRNA biology. By comparison, one of the most visually conspicuous events –how follicles take on their shape—has received little attention. As a model for morphogenesis, the follicle again offers many attractive features (Horne-Badovinac and Bilder, 2005Horne-Badovinac S. Bilder D. Mass transit: epithelial morphogenesis in the Drosophila egg chamber.Dev. Dyn. 2005; 232: 559-574Crossref PubMed Scopus (224) Google Scholar). First, after leaving the germarium, each follicle is encased in its own basement membrane, and its development can be considered as largely isolated. Second, it has well-defined and restricted periods of cell division. After the 16 cell cyst is formed, the germline grows only through endoreplication of nurse cells, which drive a >5000-fold expansion of follicle volume. Meanwhile, the follicle epithelium proliferates to ∼650–1000 cells (measurements vary) by the end of stage 6, when cell divisions cease; afterward, endoreplication allows continued FC growth (Figure 2C ). Therefore, changes in follicle shape after stage 6 are “pure” morphogenesis, with limited complicating involvement of cell proliferation or death. Third, the follicle is geometrically simple; it is radially symmetric around its anterior-posterior (A-P) axis (Figure 1D) until dorsal-ventral symmetry is broken at stage 7 (Roth and Lynch, 2009Roth S. Lynch J.A. Symmetry breaking during Drosophila oogenesis.Cold Spring Harb Perspect Biol. 2009; 1: a001891Crossref Scopus (104) Google Scholar). Indeed, the A-P axis is the early follicle's only apparent axis, evident in the presence of specialized FCs at each pole of the epithelium, with the oocyte localized to the posterior pole (Figures 1A and 1C). Fourth and most critically, the follicle undergoes a sequence of fascinating morphogenetic changes during its development. Some of these (e.g., border cell migration [Montell, 2003Montell D.J. Border-cell migration: the race is on.Nat. Rev. Mol. Cell Biol. 2003; 4: 13-24Crossref PubMed Scopus (243) Google Scholar, Rørth, 2009Rørth P. Collective cell migration.Annu. Rev. Cell Dev. Biol. 2009; 25: 407-429Crossref PubMed Scopus (390) Google Scholar], dorsal appendage morphogenesis [Berg, 2008Berg C.A. Tube formation in Drosophila egg chambers.Tissue Eng. Part A. 2008; 14: 1479-1488Crossref PubMed Scopus (24) Google Scholar]) have met with substantial previous study; others (e.g., the squamous/columnar transition of cuboidal epithelial cells and their accompanying repositioning with respect to the germline [Grammont, 2007Grammont M. Adherens junction remodeling by the Notch pathway in Drosophila melanogaster oogenesis.J. Cell Biol. 2007; 177: 139-150Crossref PubMed Scopus (41) Google Scholar, Kolahi et al., 2009Kolahi K.S. White P.F. Shreter D.M. Classen A.K. Bilder D. Mofrad M.R. Quantitative analysis of epithelial morphogenesis in Drosophila oogenesis: New insights based on morphometric analysis and mechanical modeling.Dev. Biol. 2009; 331: 129-139Crossref PubMed Scopus (44) Google Scholar]) less so. In this review we focus on the most obvious morphogenetic change, which is also the simplest: how eggs develop their oval shape. Newly formed follicles are nearly perfect spheres, which appear round in cross-section. As the follicle grows, growth is initially isotropic; stage 4 follicles are nearly as round as their precursors (Figures 1A and 2A). However, during stage 5, the follicle begins a pronounced elongation, as growth along the A-P axis exceeds that along the axes perpendicular, hereafter referred to as the “circumferential axis” (Bateman et al., 2001Bateman J. Reddy R.S. Saito H. Van Vactor D. The receptor tyrosine phosphatase Dlar and integrins organize actin filaments in the Drosophila follicular epithelium.Curr. Biol. 2001; 11: 1317-1327Abstract Full Text Full Text PDF PubMed Scopus (103) Google Scholar, Frydman and Spradling, 2001Frydman H.M. Spradling A.C. The receptor-like tyrosine phosphatase lar is required for epithelial planar polarity and for axis determination within drosophila ovarian follicles.Development. 2001; 128: 3209-3220PubMed Google Scholar, Haigo and Bilder, 2011Haigo S.L. Bilder D. Global tissue revolutions in a morphogenetic movement controlling elongation.Science. 2011; 331: 1071-1074Crossref PubMed Scopus (217) Google Scholar). At stage 7, the follicle is a prolate ellipsoid (in cross-section a fairly regular oval) (Figures 1A and 2A), a geometry that is also seen in the stage 14 (nearly mature) egg. The follicle elongates ∼2 fold (∼75% of total) in 20 hr between stages 5 and 9, which we refer to as the “major phase” of follicle elongation (Figure 2A), and by stage 10, it has reached ∼2.5 fold. At the end of stage 10, the contents of the nurse cells are transferred rapidly into the oocyte in a process called “dumping” (Mahajan-Miklos and Cooley, 1994Mahajan-Miklos S. Cooley L. Intercellular cytoplasm transport during Drosophila oogenesis.Dev. Biol. 1994; 165: 336-351Crossref PubMed Scopus (143) Google Scholar); live imaging suggests that the oocyte expands to fill existing follicle dimensions, so dumping primarily determines egg volume rather than follicle shape per se (Lee and Cooley, 2007Lee S. Cooley L. Jagunal is required for reorganizing the endoplasmic reticulum during Drosophila oogenesis.J. Cell Biol. 2007; 176: 941-952Crossref PubMed Scopus (29) Google Scholar). Ellipsoid shape represents a solution to maximize volume while passing through a narrow cross-sectional area such as an oviduct (Smart, 1991Smart I.H. Egg shape in birds.in: Deeming D.C. Ferguson M.W.J. Egg Incubation: Its Effects on Embryonic Development in Birds and Reptiles. Cambridge University Press, Cambridge1991: 101-116Crossref Google Scholar); indeed, elongation of the Drosophila egg is required for it to travel readily down the oviduct to be fertilized and laid. Moreover, as egg shape prefigures that of the fertilized zygote, it influences the diffusion of embryonic patterning gradients. Overall, the elemental geometric transitions during Drosophila egg elongation provide a simple case of organ morphogenesis. Through what mechanisms do insect eggs assume an elongated shape? Pioneering investigations were made on the Dipteran gall midge Heteropeza, whose eggs also elongate from spherical to ellipsoid during development. Removal of the follicle epithelium through irradiation, chemical, or mechanical manipulation caused spherical eggs to develop, suggesting a critical role for the epithelium in elongation (Went, 1978Went D. Oocyte maturation without follicular epithelium alters egg shape in a Dipteran insect.J. Exp. Zool. 1978; 205: 149-155Crossref Scopus (12) Google Scholar, Went and Junquera, 1981Went D.F. Junquera P. Embryonic development of insect eggs formed without follicular epithelium.Dev. Biol. 1981; 86: 100-110Crossref PubMed Scopus (13) Google Scholar). Strikingly, nearly spherical eggs are also produced by Drosophila homozygous for a female sterile mutation isolated by Nusslein-Volhard called kugelei (kug) (Figure 3E ) (Gutzeit et al., 1991Gutzeit H.O. Eberhardt W. Gratwohl E. Laminin and basement membrane-associated microfilaments in wild-type and mutant Drosophila ovarian follicles.J. Cell Sci. 1991; 100: 781-788PubMed Google Scholar) (now known as fat2, see below). The eggs of kug females are both shorter and broader than WT eggs, distinguishing them from small egg mutants that fail to undergo nurse cell dumping and emphasizing that kug induces a specific defect in organ shape. A similar, albeit weaker, phenotype is seen in short egg (seg) mutants, and activity of the seg gene product, like kug, appears to be required in the FCs and not the germline (Wieschaus et al., 1981Wieschaus E. Audit C. Masson M. A clonal analysis of the roles of somatic cells and germ line during oogenesis in Drosophila.Dev. Biol. 1981; 88: 92-103Crossref PubMed Scopus (38) Google Scholar). These data reinforce the notion that egg elongation is determined by activities in the follicle epithelium. The existence of the kug mutation indicated that egg elongation is under simple genetic control. Subsequent, often serendipitous descriptions of additional mutations that disrupt elongation of eggs or follicles—hereafter called “round egg mutants”—confirmed this finding. Some of these mutants, like kug, are homozygous viable but mutant females produce a portion of round eggs, suggesting that egg shape control is a principal role of the gene product. Other mutants show essential requirements in embryonic or larval development, and their role in egg shape is revealed through genetic mosaic analysis (Figures 3F, 3H, and 3I). To date, all tested round egg mutants act in FCs rather than the germline. Interestingly, the molecular identity of genes known to control egg elongation indicates that most act in a single process: linking the extracellular matrix to intracellular actin filaments (Figure 5D). Extracellular matrix components that are found in the follicle basement membrane include Collagen IV and Laminin; both are required for egg elongation (Frydman and Spradling, 2001Frydman H.M. Spradling A.C. The receptor-like tyrosine phosphatase lar is required for epithelial planar polarity and for axis determination within drosophila ovarian follicles.Development. 2001; 128: 3209-3220PubMed Google Scholar, Haigo and Bilder, 2011Haigo S.L. Bilder D. Global tissue revolutions in a morphogenetic movement controlling elongation.Science. 2011; 331: 1071-1074Crossref PubMed Scopus (217) Google Scholar). Mutations in receptors for these molecules that are expressed on the FC basal surface, including Integrin α and β subunits (Figure 3F), Dystroglycan, and the receptor tyrosine phosphatase Dlar, also cause the production of round eggs (Bateman et al., 2001Bateman J. Reddy R.S. Saito H. Van Vactor D. The receptor tyrosine phosphatase Dlar and integrins organize actin filaments in the Drosophila follicular epithelium.Curr. Biol. 2001; 11: 1317-1327Abstract Full Text Full Text PDF PubMed Scopus (103) Google Scholar, Deng et al., 2003Deng W.M. Schneider M. Frock R. Castillejo-Lopez C. Gaman E.A. Baumgartner S. Ruohola-Baker H. Dystroglycan is required for polarizing the epithelial cells and the oocyte in Drosophila.Development. 2003; 130: 173-184Crossref PubMed Scopus (147) Google Scholar, Duffy et al., 1998Duffy J.B. Harrison D.A. Perrimon N. Identifying loci required for follicular patterning using directed mosaics.Development. 1998; 125: 2263-2271PubMed Google Scholar, Frydman and Spradling, 2001Frydman H.M. Spradling A.C. The receptor-like tyrosine phosphatase lar is required for epithelial planar polarity and for axis determination within drosophila ovarian follicles.Development. 2001; 128: 3209-3220PubMed Google Scholar). Finally, proteins that link these extracellular matrix receptors to the actin cytoskeleton, including the integrin binding protein Talin and the Dystroglycan-binding protein Dystrophin, are required, as is the Pak kinase, which may control actin organization downstream of Dlar and integrins (Bécam et al., 2005Bécam I.E. Tanentzapf G. Lepesant J.A. Brown N.H. Huynh J.R. Integrin-independent repression of cadherin transcription by talin during axis formation in Drosophila.Nat. Cell Biol. 2005; 7: 510-516Crossref PubMed Scopus (57) Google Scholar, Conder et al., 2007Conder R. Yu H. Zahedi B. Harden N. The serine/threonine kinase dPak is required for polarized assembly of F-actin bundles and apical-basal polarity in the Drosophila follicular epithelium.Dev. Biol. 2007; 305: 470-482Crossref PubMed Scopus (48) Google Scholar, Mirouse et al., 2009Mirouse V. Christoforou C.P. Fritsch C. St Johnston D. Ray R.P. Dystroglycan and perlecan provide a basal cue required for epithelial polarity during energetic stress.Dev. Cell. 2009; 16: 83-92Abstract Full Text PDF PubMed Scopus (49) Google Scholar). Not all round egg mutants induce identical phenotypes; they vary in the frequency and degree of round eggs produced, and some display round follicles that die prior to egg production. Nevertheless, they collectively indicate that interactions between the actin cytoskeleton within FCs and the basement membrane underlying them are crucial for proper egg shape. Follicle epithelia mutant for the above genes ultimately produce round eggs, but how do these arise? Developmental analyses have generally traced defects back to the major phase of follicle elongation. For follicles lacking Dlar or integrin function, aspect ratios diverge from WT around stage 5; collagen IV mutants diverge slightly later (Bateman et al., 2001Bateman J. Reddy R.S. Saito H. Van Vactor D. The receptor tyrosine phosphatase Dlar and integrins organize actin filaments in the Drosophila follicular epithelium.Curr. Biol. 2001; 11: 1317-1327Abstract Full Text Full Text PDF PubMed Scopus (103) Google Scholar, Frydman and Spradling, 2001Frydman H.M. Spradling A.C. The receptor-like tyrosine phosphatase lar is required for epithelial planar polarity and for axis determination within drosophila ovarian follicles.Development. 2001; 128: 3209-3220PubMed Google Scholar, Haigo and Bilder, 2011Haigo S.L. Bilder D. Global tissue revolutions in a morphogenetic movement controlling elongation.Science. 2011; 331: 1071-1074Crossref PubMed Scopus (217) Google Scholar). Analysis of mutant follicles at these stages has revealed that they all share a common phenotype. The follicles that fail to elongate display defects in a striking planar polarized organization of actin filaments on the basal surface of the follicle epithelium (Figures 3A and 3B). Planar polarity refers to the organization of morphological and/or molecular structures within and/or across a tissue in a plane orthogonal to its apicobasal axis (note that this term is meant to be more general than the commonly used “planar cell polarity” [Goodrich and Strutt, 2011Goodrich L.V. Strutt D. Principles of planar polarity in animal development.Development. 2011; 138: 1877-1892Crossref PubMed Scopus (423) Google Scholar]). The first description of this organization in Drosophila ovaries came when Gutzeit, following earlier studies on microtubules in Heteropeza, documented basally localized arrays of parallel actin filaments in FCs (Gutzeit, 1990Gutzeit H.O. The microfilament pattern in the somatic follicle cells of mid-vitellogenic ovarian follicles of Drosophila.Eur. J. Cell Biol. 1990; 53: 349-356PubMed Google Scholar, Tucker and Meats, 1976Tucker J.B. Meats M. Microtubules and control of insect egg shape.J. Cell Biol. 1976; 71: 207-217Crossref PubMed Scopus (41) Google Scholar) that show three aspects of planar polarity. First, all filaments within an individual cell show a common orientation. Second, in all cells this orientation is coordinated; they are aligned around the circumferential axis of the follicle, perpendicular to the elongating A-P axis. Third, on one face along the circumferential axis, filaments in one cell terminate in filopodia-like protrusions that cross over to neighboring cells (Figures 3A and 3J). These features, particularly the monopolar protrusions, prompted Gutzeit (Gutzeit, 1991Gutzeit H.O. Organization and in vitro activity of microfilament bundles associated with the basement membrane of Drosophila follicles.Acta Histochem. Suppl. 1991; 41: 201-210PubMed Google Scholar) to term this organization “planar circular polarity”; we prefer the term “chiral planar polarity” to distinguish the oriented but continuous planar polarity of the follicle from the more familiar planar polarity seen in bounded tissues. Planar polarized organization is not apparent when the follicle exits the germarium; consistently oriented basal actin filaments are not visible at stage 4. However, during stage 5 long and thin actin filaments appear along FC basal surfaces, oriented circumferentially, and become increasingly robust until late stage 8 (Figures 3A and 3J), after which they become disorganized as the FCs undergo further morphogenetic events (Figures 2B and 2C) (Bateman et al., 2001Bateman J. Reddy R.S. Saito H. Van Vactor D. The receptor tyrosine phosphatase Dlar and integrins organize actin filaments in the Drosophila follicular epithelium.Curr. Biol. 2001; 11: 1317-1327Abstract Full Text Full Text PDF PubMed Scopus (103) Google Scholar, Delon and Brown, 2009Delon I. Brown N.H. The integrin adhesion complex changes its composition and function during morphogenesis of an epithelium.J. Cell Sci. 2009; 122: 4363-4374Crossref PubMed Scopus (51) Google Scholar, Frydman and Spradling, 2001Frydman H.M. Spradling A.C. The receptor-like tyrosine phosphatase lar is required for epithelial planar polarity and for axis determination within drosophila ovarian follicles.Development. 2001; 128: 3209-3220PubMed Google Scholar, Gutzeit, 1990Gutzeit H.O. The microfilament pattern in the somatic follicle cells of mid-vitellogenic ovarian follicles of Drosophila.Eur. J. Cell Biol. 1990; 53: 349-356PubMed Google Scholar, He et al., 2010He L. Wang X.B. Tang H.L. Montell D.J. Tissue elongation requires oscillating contractions of a basal actomyosin network.Nat. Cell Biol. 2010; 12: 1133-1142Crossref PubMed Scopus (183) Google Scholar). Planar polarized actin organization reappears transiently at stage 10A and then more stably at stage 12, when filaments in oocyte-contacting FCs form dense polarized bundles that occupy most of basal surface. The latter show striking morphological and molecular resemblances to focal adhesions seen in cell culture (Figure 3B) (Delon and Brown, 2009Delon I. Brown N.H. The integrin adhesion complex changes its composition and function during morphogenesis of an epithelium.J. Cell Sci. 2009; 122: 4363-4374Crossref PubMed Scopus (51) Google Scholar). Does planar polarized actin organization play a role in Drosophila egg elongation? Tucker and Meats initially suggested that mechanical properties of a planar polarized cytoskeleton in insect follicles might constrain growth along the circumferential axis, by providing “greater resistance to circumferential expansion than to elongation of the follicle parallel to its polar axis” (Tucker and Meats, 1976Tucker J.B. Meats M. Microtubules and control of insect egg shape.J. Cell Biol. 1976; 71: 207-217Crossref PubMed Scopus (41) Google Scholar). This model found some favor with subsequent investigators, who termed it a “molecular corset.” Experimental support for an actin-based molecular corset came from analyzing “round egg” mutant follicles (Bateman et al., 2001Bateman J. Reddy R.S. Saito H. Van Vactor D. The receptor tyrosine phosphatase Dlar and integrins organize actin filaments in the Drosophila follicular epithelium.Curr. Biol. 2001; 11: 1317-1327Abstract Full Text Full Text PDF PubMed Scopus (103) Google Scholar, Conder et al., 2007Conder R. Yu H. Zahedi B. Harden N. The serine/threonine kinase dPak is required for polarized assembly of F-actin bundles and apical-basal polarity in the Drosophila follicular epithelium.Dev. Biol. 2007; 305: 470-482Crossref PubMed Scopus (48) Google Scholar, Frydman and Spradling, 2001Frydman H.M. Spradling A.C. The receptor-like tyrosine phosphatase lar is required for epithelial planar polarity and for axis determination within drosophila ovarian follicles.Development. 2001; 128: 3209-3220PubMed Google Scholar, Gutzeit et al., 1991Gutzeit H.O. Eberhardt W. Gratwohl E. Laminin and basement membrane-associated microfilaments in wild-type and mutant Drosophila ovarian follicles.J. Cell Sci. 1991; 100: 781-788PubMed Google Scholar, Viktorinová et al., 2009Viktorinová I. König T. Schlichting K. Dahmann C. The cadherin Fat2 is required for planar cell polarity in the Drosophila ovary.Development. 2009; 136: 4123-4132Crossref PubMed Scopus (82) Google Scholar). In these, actin filaments retained a common orientation within a given FC, but the orientation in each cell was mispolarized with respect to the follicle axis (Figure 3G). This loss of polarity is reminiscent of that seen in mutations that disrupt planar polarity in widely studied systems such as the fly wing and vertebrate inner ear (Axelrod, 2009Axelrod J.D. Progress and challenges in understanding planar cell polarity signaling.Semin. Cell Dev. Biol. 2009; 20: 964-971Crossref PubMed Scopus (105) Google Scholar, Goodrich and Strutt, 2011Goodrich L.V. Strutt D. Principles of planar polarity in animal development.Development. 2011; 138: 1877-1892Crossref PubMed Scopus (423) Google Scholar) where polarity is controlled by genes such as frizzled, dishevelled, fat, and dachsous (which we call here the “conventional PCP signaling pathways,” Figures 5A and 5B). Other resemblances suggested a link between the two phenomena. For instance, planar polarity in “round egg” mutant follicles is not random but appears influenced by neighboring cells, with signs of swirls and regional organization. Moreover, mosaic analysis shows that a patch of such mutant FCs can non-cell-autonomously alter the polarity of WT neighbors (Figures 3H and 3I) (Bateman et al., 2001Bateman J. Reddy R.S. Saito H. Van Vactor D. The receptor tyrosine phosphatase Dlar and integrins organize actin filaments in the Drosophila follicular epithelium.Curr. Biol. 2001; 11: 1317-1327Abstract Full Text Full Text PDF PubMed Scopus (103) Google Scholar, Frydman and Spradling, 2001Frydman H.M. Spradling A.C. The receptor-like tyrosine phosphatase lar is required for epithelial planar polarity and for axis determination within drosophila ovarian follicles.Development. 2001; 128: 3209-3220PubMed Google Scholar, Viktorinová et al., 2009Viktorinová I. König T. Schlichting K. Dahmann C. The cadherin Fat2 is required for planar cell polarity in the Drosophila ovary.Development. 2009; 136: 4123-4132Crossref PubMed Scopus (82) Google Scholar). Despite the several similarities between planar polarity in the follicle and in more familiar planar polarized systems, there are also notable differences. Though both can regulate the polarization of actin-based structures within the plane of an epithelium, conventional PCP signaling often controls actin at the apical surface while in the follicle polarity is manifested at the basal surface. Mutations that disrupt conventional PCP signaling show cell-autonomous phenotypes in clones of cells; there is little nonautonomous rescue. By contrast, small clones of round egg mutant cells can show no disruption of polarity, while large clones do. Finally, mutations that disrupt conventional PCP regulators such as Dishevelled, Van Gogh, Fat, and Dachsous have no apparent effect on follicle actin organization or elongation (Viktorinová et al., 2009Viktorinová I. König T. Schlichting K. Dahmann C. The cadherin Fat2 is required for planar cell polarity in the Drosophila ovary.Development. 2009; 136: 4123-4132Crossref PubMed Scopus (82) Google Scholar), suggesting that a different molecular pathway is involved in controlling planar polarity in the follicle. Potential insight into an alternative follicle planar polarity pathway has come from the recent identification of a new egg elongation regulator (Viktorinová et al., 2009Viktorinová I. König T. Schlichting K. Dahmann C. The cadherin Fat2 is required for planar cell polarity in the Drosophila ovary.Development. 2009; 136: 4123-4132Crossref PubMed Scopus (82) Google Scholar). Fat2 encodes a large atypical cadherin that is related to Fat, an important regulator of conventional PCP signaling in fly wings, eyes, and abdomen. Reverse genetic analysis of using small chromosomal deletions revealed that flies lacking Fat2 are viable but female sterile and only produce round eggs, similar" @default.
• W1993676881 created "2016-06-24" @default.
• W1993676881 creator A5062920414 @default.
• W1993676881 creator A5074070755 @default.
• W1993676881 date "2012-01-01" @default.
• W1993676881 modified "2023-10-12" @default.
• W1993676881 title "Expanding the Morphogenetic Repertoire: Perspectives from the Drosophila Egg" @default.
• W1993676881 cites W191629038 @default.
• W1993676881 cites W1966078124 @default.
• W1993676881 cites W1967120404 @default.
• W1993676881 cites W1969883800 @default.
• W1993676881 cites W1974084078 @default.
• W1993676881 cites W1974210089 @default.
• W1993676881 cites W1974296262 @default.
• W1993676881 cites W1978789471 @default.
• W1993676881 cites W1979351753 @default.
• W1993676881 cites W1980908755 @default.
• W1993676881 cites W1982204785 @default.
• W1993676881 cites W1984708173 @default.
• W1993676881 cites W1987817703 @default.
• W1993676881 cites W1989723819 @default.
• W1993676881 cites W1993199560 @default.
• W1993676881 cites W1998463412 @default.
• W1993676881 cites W1998481526 @default.
• W1993676881 cites W2001236385 @default.
• W1993676881 cites W2004201883 @default.
• W1993676881 cites W2005154637 @default.
• W1993676881 cites W2005387062 @default.
• W1993676881 cites W2008127822 @default.
• W1993676881 cites W2010043731 @default.
• W1993676881 cites W2010995441 @default.
• W1993676881 cites W2018207596 @default.
• W1993676881 cites W2027179352 @default.
• W1993676881 cites W2030274279 @default.
• W1993676881 cites W2031721857 @default.
• W1993676881 cites W2035018334 @default.
• W1993676881 cites W2036779499 @default.
• W1993676881 cites W2038572636 @default.
• W1993676881 cites W2042096731 @default.
• W1993676881 cites W2053251449 @default.
• W1993676881 cites W2056922353 @default.
• W1993676881 cites W2057854872 @default.
• W1993676881 cites W2060058003 @default.
• W1993676881 cites W2060114324 @default.
• W1993676881 cites W2068641012 @default.
• W1993676881 cites W2070269730 @default.
• W1993676881 cites W2071051512 @default.
• W1993676881 cites W2075234068 @default.
• W1993676881 cites W2078164530 @default.
• W1993676881 cites W2079595896 @default.
• W1993676881 cites W2080156358 @default.
• W1993676881 cites W2082686158 @default.
• W1993676881 cites W2086811477 @default.
• W1993676881 cites W2089593631 @default.
• W1993676881 cites W2091884095 @default.
• W1993676881 cites W2095658523 @default.
• W1993676881 cites W2099316631 @default.
• W1993676881 cites W2100667554 @default.
• W1993676881 cites W2110995655 @default.
• W1993676881 cites W2111600440 @default.
• W1993676881 cites W2115758207 @default.
• W1993676881 cites W2124073775 @default.
• W1993676881 cites W2127367210 @default.
• W1993676881 cites W2127481925 @default.
• W1993676881 cites W2127783917 @default.
• W1993676881 cites W2129557429 @default.
• W1993676881 cites W2130255071 @default.
• W1993676881 cites W2130735747 @default.
• W1993676881 cites W2130793174 @default.
• W1993676881 cites W2132756167 @default.
• W1993676881 cites W2134160463 @default.
• W1993676881 cites W2135553987 @default.
• W1993676881 cites W2136840646 @default.
• W1993676881 cites W2142337477 @default.
• W1993676881 cites W2144792264 @default.
• W1993676881 cites W2145013849 @default.
• W1993676881 cites W2145232323 @default.
• W1993676881 cites W2146098038 @default.
• W1993676881 cites W2148123685 @default.
• W1993676881 cites W2159952016 @default.
• W1993676881 cites W2166143596 @default.
• W1993676881 cites W2166254523 @default.
• W1993676881 cites W2239723008 @default.
• W1993676881 cites W2276527648 @default.
• W1993676881 cites W4245446181 @default.
• W1993676881 doi "https://doi.org/10.1016/j.devcel.2011.12.003" @default.
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