1 This trade-off is driven by the size of the
ommatidial acceptance angle.
2 This doubled the
ommatidial acceptance angles and increased microvillar s
3 z thus bring about the concerted assembly of
ommatidial and synaptic cartridge units, imposing the "n
4 at mutants show increased local variation in
ommatidial area, which is sufficient to induce a signifi
5 ment with N5NM15 and PAA did not improve the
ommatidial arrangement, eye bristle count, or eye length
6 of the adult eye surface, causes defects in
ommatidial assembly and ommatidial spacing.
7 The EGFR ligand Spitz, a signal for
ommatidial assembly in the compound eye, is transported
8 disposes ommatidial precursor cells to enter
ommatidial assembly later.
9 lls may further contribute to the defects in
ommatidial assembly.
10 revealing that OR is driven autonomously by
ommatidial cell clusters rotating in successive pulses w
11 ts occurs at the same time as the peripheral
ommatidial cell death and also depends on head involutio
12 vity is essential for establishing the first
ommatidial cell fate, the R8 photoreceptor neuron.
13 cell divisions that overlaps early stages of
ommatidial cell specification.
14 neighboring ommatidia are separated by inter-
ommatidial cells (IOCs).
15 actors are expressed only in a subset of the
ommatidial cells not including the photoreceptors.
16 m, and generating this 3D structure requires
ommatidial cells to adopt specific apical and basal poly
17 Zip is also robust in newly added
ommatidial cells, consistent with our model that the mac
18 amacrochaetae (Emc) leads to defects in both
ommatidial chirality and rotation.
19 e use in situ hybridization to visualize six
ommatidial classes in the compound eye of a lycaenid but
20 for normal morphogenetic furrow movement and
ommatidial cluster formation.
21 Surprisingly, there is no loss of
ommatidial clusters in senseless mutant tissue and all o
22 sembly of photoreceptor precursor cells into
ommatidial clusters in the compound eye.
23 e specification and organization of immature
ommatidial clusters occur in conjunction with furrow pro
24 anteriorly, additional asymmetry develops as
ommatidial clusters rotate coordinately in opposite dire
25 DAB is expressed in the
ommatidial clusters, and loss of DAB function disrupts o
26 R4, R7 and cone cell types, and rotation of
ommatidial clusters.
27 tially recruited into each of the developing
ommatidial clusters.
28 sca protein control the pattern of the next
ommatidial column.
29 is a highly conserved protein present in the
ommatidial crystallin cone and central nervous system of
30 actors in the eye periphery that directs the
ommatidial death and subsequent PR formation.
31 echanical stiffness providing constraints to
ommatidial deformation and thus to defect generation.
32 gressive loss of dopaminergic neurons and in
ommatidial degeneration of the compound eye, which is re
33 nts SOD and vitamin E significantly inhibits
ommatidial degeneration.
34 Delivery to the retina propagates
ommatidial development across a precursor field.
35 Its localization is dynamic throughout
ommatidial development and is dependent on Frizzled and
36 We show further that Hh induces
ommatidial development in the absence of its secondary s
37 clusters, and loss of DAB function disrupts
ommatidial development.
38 proneural clusters during the initiation of
ommatidial differentiation in the developing eye disc.
39 The advancing front of
ommatidial differentiation is marked by the morphogeneti
40 ic backgrounds and new mutations that affect
ommatidial differentiation, morphology or chirality.
41 Myc on growth, cell death, and inhibition of
ommatidial differentiation.
42 tion is the repression of wg, which prevents
ommatidial differentiation.
43 aginal disc into a near crystalline array of
ommatidial elements.
44 ive, grim and reaper, which are required for
ommatidial elimination.
45 es a pool of uncommitted cells used for most
ommatidial fates.
46 50 plays a critical role in regulating early
ommatidial formation.
47 zed arrangement of dorsal and ventral chiral
ommatidial forms.
48 is responsible for the specification of the
ommatidial founder cells R8.
49 e in the initial specification or spacing of
ommatidial founder cells.
50 their correct shape and position within the
ommatidial hexagon.
51 indings establish that SJs are essential for
ommatidial integrity and in creating a BEB around the io
52 ed in the rough-eye phenotype with disrupted
ommatidial lattice and reduced number of photoreceptor c
53 The regular organization of the
ommatidial lattice in the Drosophila eye originates in t
54 hemistry reveals the presence of rudimentary
ommatidial lenses, crystalline cones, and associated neu
55 with early diagenetic mineralization of the
ommatidial lenses.
56 f 20E required for furrow progression versus
ommatidial maturation differ by about 17-fold.
57 Ommatidial maturation normally occurs after the furrow h
58 hows that loss of Nrx IV leads to defects in
ommatidial morphology and integrity.
59 sary and sufficient for the formation of the
ommatidial mosaic.
60 to one another in a pattern that prefigures
ommatidial organisation in the mature compound eye.
61 The overall conserved
ommatidial organization and R7 retinal patterning show t
62 Scanning electron microscopy documents
ommatidial organization of these induced structures, whi
63 MO/CED-12 in the eye causes perturbations in
ommatidial organization that are suppressed by mutations
64 r of novel, functionally relevant aspects of
ommatidial organization that have not previously been de
65 eir final position, and that in its absence,
ommatidial orientation becomes disrupted during the remo
66 ly boundary irregularities, ensuring uniform
ommatidial packing that is critical for precise optical
67 akdown of this perfect symmetry, so that the
ommatidial pattern shows onset of disorder in the form o
68 crane-flies, in which it forms the outermost
ommatidial pigment shield in compound eyes incorporating
69 components, could pattern hair, bristle and
ommatidial planar polarity in Drosophila, and that addit
70 our-jointed function resulted in only a mild
ommatidial polarity defect.
71 our-jointed are consistent with it acting in
ommatidial polarity determination as a second signal dow
72 ment, and the truncated form of DFz2 affects
ommatidial polarity during eye development.
73 ndent in the wing disc and additionally that
ommatidial polarity in the eye can be determined without
74 lay defects in photoreceptor recruitment and
ommatidial polarity in the eye.
75 resulted in strong non-autonomous defects in
ommatidial polarity on the dorsoventral axis.
76 The
ommatidial polarity phenotypes of rin are similar to tho
77 vity across the DV axis of the eye regulates
ommatidial polarity via an unidentified second signal.
78 required at the time during development when
ommatidial polarity was being determined.
79 ectopic eye field and the reorganization of
ommatidial polarity, and ubiquitous pannier expression c
80 input in R3 or R4 to establish cell fate and
ommatidial polarity.
81 uired in R3 for the establishment of correct
ommatidial polarity.
82 function to regulate wing hair, bristle and
ommatidial polarity.
83 tonomously required for the establishment of
ommatidial polarity.
84 for the establishment of the equator and of
ommatidial polarity.
85 onsistent with it mediating their effects on
ommatidial polarity.
86 embly is directed by cells within developing
ommatidial preclusters.
87 the initiation of patterning and predisposes
ommatidial precursor cells to enter ommatidial assembly
88 mmatidial rotation to modulate the degree of
ommatidial precursor movement.
89 scs, ommatidial rotation is delayed and some
ommatidial precursors initiate rotation in the wrong dir
90 rotation to regulate the speed at which the
ommatidial precursors move.
91 l disc as cells adopt their fates and as the
ommatidial precursors undergo coordinated rotation withi
92 ees rotational movement of the multicellular
ommatidial precursors within a matrix of stationary cell
93 is confirms that these subsets of cells, the
ommatidial precursors, do stall at 45 degrees , we demon
94 otational movements of subsets of cells, the
ommatidial precursors, establish mirror symmetry in the
95 a is largely normal, defects are observed in
ommatidial rotation (OR), a planar cell polarity (PCP)-m
96 Ommatidial rotation (OR), directed by planar cell polari
97 pattern is established and how it relates to
ommatidial rotation are unknown.
98 ation of a requirement for cone cells in the
ommatidial rotation aspect of PCP.
99 a new role of Egfr signaling in controlling
ommatidial rotation during planar cell polarity (PCP) es
100 which differentiation initiates, and direct
ommatidial rotation in opposite directions in the two ha
101 Ommatidial rotation in the Drosophila eye provides a str
102 h of the planar polarity pathway involved in
ommatidial rotation in the eye and in restricting actin
103 Ommatidial rotation is a cell motility read-out of plana
104 In stbm eye discs,
ommatidial rotation is delayed and some ommatidial precu
105 d, the mechanistic aspects of the associated
ommatidial rotation process remain unknown.
106 and Friend of Echinoid (Fred) act throughout
ommatidial rotation to modulate the degree of ommatidial
107 Defects in chirality and/or
ommatidial rotation will lead to disorganization of the
108 Wing hair alignment and
ommatidial rotation, functional readouts of planar cell
109 , is required in R7 to control the degree of
ommatidial rotation.
110 modulation of Egfr activity shows defects in
ommatidial rotation.
111 we show that Hth expression expands to many
ommatidial rows in regulatory mutants of optomotorblind
112 how the DRA is limited to exactly one or two
ommatidial rows is not known.
113 Wave intensity scales with
ommatidial size, triggering stronger myosin II-driven ap
114 The initial
ommatidial spacing at the furrow occurs normally in the
115 The
ommatidial spacing defect can be ascribed to the irregul
116 How this
ommatidial spacing emerges during eye development is not
117 er Rst or Kirre alone had minimal effects on
ommatidial spacing, but reducing both together led to di
118 e, causes defects in ommatidial assembly and
ommatidial spacing.
119 es to activate rh3 and rh5 in their specific
ommatidial subclass and through the same sites to preven
120 ilar to the human cone photoreceptors, these
ommatidial subtypes are distributed stochastically in th
121 ing changes in other coordinated features of
ommatidial type.
122 mes of Spineless expression define the three
ommatidial types in butterflies.
123 ad generate three stochastically distributed
ommatidial types, resulting in a more diverse retinal mo
124 And we have learned that each
ommatidial unit is involved in the life-death decision o
125 events that occur during pupal life move the
ommatidial units an additional 15 degrees.
126 organized pupal lattice, in which hexagonal
ommatidial units pack tightly.