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1

England, Samantha J., and Richard J. Adams. "Building a dynamic fate map." BioTechniques 43, no. 1S (July 2007): S20—S24. http://dx.doi.org/10.2144/000112510.

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2

Schnittger, Arp, Paul E. Grini, Ulrike Folkers, and Martin Hülskamp. "Epidermal Fate Map of theArabidopsisShoot Meristem." Developmental Biology 175, no. 2 (May 1996): 248–55. http://dx.doi.org/10.1006/dbio.1996.0112.

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3

Waldron, Denise. "A colourful map of cell fate." Nature Reviews Genetics 17, no. 5 (April 4, 2016): 252. http://dx.doi.org/10.1038/nrg.2016.48.

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4

Woodrick, R., P. R. Martin, I. Birman, and F. B. Pickett. "The Arabidopsis embryonic shoot fate map." Development 127, no. 4 (February 15, 2000): 813–20. http://dx.doi.org/10.1242/dev.127.4.813.

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A fate map has been constructed for the shoot apical region of the embryo of the dicotyledonous plant Arabidopsis thaliana using spontaneously arising clonal albino sectors caused by the chloroplast mutator 1–2 mutation. Chimeric seedlings exhibiting albino sectors shared between the cotyledons and first true leaves revealed patterns of organ inclusion and exclusion. Frequencies of clone sharing were used to calculate developmental distances between organs based on the frequency of clonal sectors failing to extend between different organs. The resulting fate map shows asymmetry in the developmental distances between the cotyledons (embryonic leaves) which in turn predicts the location of the first post-germination leaf and the handedness of the spiral of leaf placement around the central stem axis in later development. The map suggests that embryonic leaf fate specification in the cotyledons may represent a developmental ground state necessary for the formation of the shoot apical meristem.
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5

Kimmel, C. B., R. M. Warga, and T. F. Schilling. "Origin and organization of the zebrafish fate map." Development 108, no. 4 (April 1, 1990): 581–94. http://dx.doi.org/10.1242/dev.108.4.581.

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We have analyzed lineages of cells labeled by intracellular injection of tracer dye during early zebrafish development to learn when cells become allocated to particular fates during development, and how the fate map is organized. The earliest lineage restriction was described previously, and segregates the yolk cell from the blastoderm in the midblastula. After one or two more cell divisions, the lineages of epithelial enveloping layer (EVL) cells become restricted to generate exclusively periderm. Following an additional division in the late blastula, deep layer (DEL) cells generate clones that are restricted to single deep embryonic tissues. The appearance of both the EVL and DEL restrictions could be causally linked to blastoderm morphogenesis during epiboly. A fate map emerges as the DEL cell lineages become restricted in the late blastula. It is similar in organization to that of an amphibian embryo. DEL cells located near the animal pole of the early gastrula give rise to ectodermal fates (including the definitive epidermis). Cells located near the blastoderm margin give rise to mesodermal and endodermal fates. Dorsal cells in the gastrula form dorsal and anterior structures in the embryo, and ventral cells in the gastrula form dorsal, ventral and posterior structures. The exact locations of progenitors of single cell types and of local regions of the embryo cannot be mapped at the stages we examined, because of variable cell rearrangements during gastrulation.
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6

Namba, R., T. M. Pazdera, R. L. Cerrone, and J. S. Minden. "Drosophila embryonic pattern repair: how embryos respond to bicoid dosage alteration." Development 124, no. 7 (April 1, 1997): 1393–403. http://dx.doi.org/10.1242/dev.124.7.1393.

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The product of the maternal effect gene, bicoid (bcd), is a transcription factor that acts in a concentration-dependent fashion to direct the establishment of anterior fates in the Drosophila melanogaster embryo. Embryos laid by mothers with fewer or greater than the normal two copies of bcd show initial alterations in the expression of the gap, segmentation and segment polarity genes, as well as changes in early morphological markers. In the absence of a fate map repair system, one would predict that these initial changes would result in drastic changes in the shape and size of larval and adult structures. However, these embryos develop into relatively normal larvae and adults. This indicates that there is plasticity in Drosophila embryonic development along the anterior-posterior axis. Embryos laid by mothers with six copies of bcd have reduced viability, indicating a threshold for repairing anterior-posterior mispatterning. We show that cell death plays a major role in correcting expanded regions of the fate map. There is a concomitant decrease of cell death in compressed regions of the fate map. We also show that compression of the fate map does not appear to be repaired by the induction of new cell divisions. In addition, some tissues are more sensitive to fate map compression than others.
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7

Zilles, Karl, and Katrin Amunts. "Centenary of Brodmann's map — conception and fate." Nature Reviews Neuroscience 11, no. 2 (January 4, 2010): 139–45. http://dx.doi.org/10.1038/nrn2776.

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8

Sebo, Zachary L., Elise Jeffery, Brandon Holtrup, and Matthew S. Rodeheffer. "A mesodermal fate map for adipose tissue." Development 145, no. 17 (July 25, 2018): dev166801. http://dx.doi.org/10.1242/dev.166801.

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9

Sanchez-Guardado, L. O., L. Puelles, and M. Hidalgo-Sanchez. "Fate map of the chicken otic placode." Development 141, no. 11 (May 12, 2014): 2302–12. http://dx.doi.org/10.1242/dev.101667.

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10

Xiao, T. T., S. Schilderink, S. Moling, E. E. Deinum, E. Kondorosi, H. Franssen, O. Kulikova, A. Niebel, and T. Bisseling. "Fate map of Medicago truncatula root nodules." Development 141, no. 18 (September 2, 2014): 3517–28. http://dx.doi.org/10.1242/dev.110775.

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11

Saulsberry, Alexandria, Paula R. Martin, Tim O’Brien, Leslie E. Sieburth, and F. Bryan Pickett. "The induced sector Arabidopsis apical embryonic fate map." Development 129, no. 14 (July 15, 2002): 3403–10. http://dx.doi.org/10.1242/dev.129.14.3403.

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Creation of an embryonic fate map may provide insight into the patterns of cell division and specification contributing to the apical region of the early Arabidopsis embryo. A fate map has been constructed by inducing genetic chimerism during the two-apical-cell stage of embryogenesis to determine if the orientation of the first anticlinal cell division correlates with later developmental axes. Chimeras were also used to map the relative locations of precursors of the cotyledon and leaf primordia. Genetic chimeras were induced in embryos doubly heterozygous for a heat shock regulated Cre recombinase and a constitutively expressed β-glucuronidase (GUS) gene flanked by the loxP binding sites for Cre. Individual cells in the two-apical-cell stage embryo responding to heat shock produce GUS-negative daughter cells. Mature plants grown from seed derived from treated embryos were scored for GUS-negative sector extent in the cotyledons and leaves. The GUS-negative daughters of apical cells had a strong tendency to contribute primarily to one cotyledon or the other and to physically adjacent true leaf margins. This result indicated that patterns of early cell division correlate with later axes of symmetry in the embryo and that these patterns partially limit the fates available for adoption by daughter cells. However, GUS-negative sectors were shared between all regions of the mature plant, suggesting that there is no strict fate restriction imposed on the daughters of the first apical cells.
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12

Redkar, Abhay, Michael Montgomery, and Judith Litvin. "Fate map of early avian cardiac progenitor cells." Development 128, no. 12 (June 15, 2001): 2269–79. http://dx.doi.org/10.1242/dev.128.12.2269.

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Cardiogenic fate maps are used to address questions on commitment, differentiation, morphogenesis and organogenesis of the heart. Recently, the accuracy of classical cardiogenic fate maps has been questioned, raising concerns about the conclusions drawn in studies based on these maps. We present accurate fate maps of the heart-forming region (HFR) in avian embryos and show that the putative cardiogenic molecular markers Bmp2 and Nkx2.5 do not govern the boundaries of the HFR as suggested in the literature. Moreover, this paper presents the first fate map of the HFR at stage 4 and addresses a void in the literature concerning rostrocaudal patterning of heart cells between stages 4 and 8.
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13

Garcia-Lopez, Raquel, Ana Pombero, and Salvador Martinez. "Fate map of the chick embryo neural tube." Development, Growth & Differentiation 51, no. 3 (March 30, 2009): 145–65. http://dx.doi.org/10.1111/j.1440-169x.2009.01096.x.

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14

Russek-Blum, Niva, Helit Nabel-Rosen, and Gil Levkowitz. "High resolution fate map of the zebrafish diencephalon." Developmental Dynamics 238, no. 7 (July 2009): 1827–35. http://dx.doi.org/10.1002/dvdy.21987.

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15

Christianson, M. L. "FATE MAP OF THE ORGANIZING SHOOT APEX IN GOSSYPIUM." American Journal of Botany 73, no. 7 (July 1986): 947–58. http://dx.doi.org/10.1002/j.1537-2197.1986.tb08538.x.

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16

Malaska, Michael J., Rosaly M. Lopes, Alex G. Hayes, Jani Radebaugh, Ralph D. Lorenz, and Elizabeth P. Turtle. "Material transport map of Titan: The fate of dunes." Icarus 270 (May 2016): 183–96. http://dx.doi.org/10.1016/j.icarus.2015.09.029.

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17

Sander, Klaus. "When seeing is believing: Wilhelm Roux's misconceived fate map." Roux's Archives of Developmental Biology 200, no. 4 (September 1991): 177–79. http://dx.doi.org/10.1007/bf00361334.

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18

Dale, L., and J. M. Slack. "Fate map for the 32-cell stage of Xenopus laevis." Development 99, no. 4 (April 1, 1987): 527–51. http://dx.doi.org/10.1242/dev.99.4.527.

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A complete fate map has been produced for the 32-cell stage of Xenopus laevis. Embryos with a regular cleavage pattern were selected and individual blastomeres were injected with the lineage label fluorescein-dextran-amine (FDA). The spatial location of the clones was deduced from three-dimensional (3D) reconstructions of later stages and the volume of each tissue colonized by labelled cells in each tissue was measured. The results from 107 cases were pooled to give a fate map which shows the fate of each blastomere in terms of tissue types, the composition of each tissue by blastomere, the location of each prospective region on the embryo and the fate of each blastomere in terms of spatial localization. Morphogenetic movements up to stage 10 (early gastrula) were assessed by carrying out a number of orthotopic grafts at blastula and gastrula stages using donor embryos uniformly labelled with FDA. Although there is a regular topographic projection from the 32-cell stage this varies a little between individuals because of variability of positions of cleavage planes and because of short-range cell mixing during gastrulation. The cell mixing means that the topographic projection fails for anteroposterior segments of the dorsal axial structures and it is not possible to include short segments of notochord or neural tube or individual somites on the pregastrulation fate map.
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19

Krispin, S., E. Nitzan, Y. Kassem, and C. Kalcheim. "Evidence for a dynamic spatiotemporal fate map and early fate restrictions of premigratory avian neural crest." Development 137, no. 4 (January 28, 2010): 585–95. http://dx.doi.org/10.1242/dev.041509.

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20

Tamnanloo, Farzaneh, Hassan Damen, Raman Jangra, and Jin Suk Lee. "MAP KINASE PHOSPHATASE1 Controls Cell Fate Transition during Stomatal Development." Plant Physiology 178, no. 1 (July 12, 2018): 247–57. http://dx.doi.org/10.1104/pp.18.00475.

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21

Cui, Cheng, Tracey J. Cheuvront, Rusty D. Lansford, Ricardo A. Moreno-Rodriguez, Thomas M. Schultheiss, and Brenda J. Rongish. "Dynamic positional fate map of the primary heart-forming region." Developmental Biology 332, no. 2 (August 2009): 212–22. http://dx.doi.org/10.1016/j.ydbio.2009.05.570.

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22

Strehlow, David, and Walter Gilbert. "A fate map for the first cleavages of the zebrafish." Nature 361, no. 6411 (February 1993): 451–53. http://dx.doi.org/10.1038/361451a0.

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23

Kale, V. P. "MAP Kinase: A Switch in Fate Determination of Stem Cells." Stem Cells and Development 14, no. 3 (June 2005): 248–51. http://dx.doi.org/10.1089/scd.2005.14.248.

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24

Irish, V. F., and I. M. Sussex. "A fate map of the Arabidopsis embryonic shoot apical meristem." Development 115, no. 3 (July 1, 1992): 745–53. http://dx.doi.org/10.1242/dev.115.3.745.

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We have mapped the fate of cells in the Arabidopsis embryonic shoot apical meristem by irradiating seed and scoring the resulting clonally derived sectors. 176 white, yellow, pale green or variegated sectors were identified and scored for their position and extent in the resulting plants. Most sectors were confined to a fraction of a leaf, and only occasionally extended into the inflorescence. Sectors that extended into the inflorescence were larger, and usually encompassed about a third to a half of the inflorescence circumference. We also find that axillary buds in Arabidopsis are clonally related to the subtending leaf. Sections through the dry seed embryo indicate that the embryonic shoot apical meristem contains approximately 110 cells in the three meristematic layers prior to the formation of the first two leaf primordia. The histological analysis of cell number in the shoot apical meristem, in combination with the sector analysis have been used to construct a map of the probable fate of cells in the embryonic shoot apical meristem.
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25

Fernández-Garre, Pedro, Lucia Rodríguez-Gallardo, Victoria Gallego-Díaz, Ignacio S. Alvarez, and Luis Puelles. "Fate map of the chicken neural plate at stage 4." Development 129, no. 12 (June 15, 2002): 2807–22. http://dx.doi.org/10.1242/dev.129.12.2807.

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A detailed fate map was obtained for the early chick neural plate (stages 3d/4). Numerous overlapping plug grafts were performed upon New-cultured chick embryos, using fixable carboxyfluorescein diacetate succinimidyl ester to label donor chick tissue. The specimens were harvested 24 hours after grafting and reached in most cases stages 9-11 (early neural tube). The label was detected immunocytochemically in wholemounts, and cross-sections were later obtained. The positions of the graft-derived cells were classified first into sets of purely neural, purely non-neural and mixed grafts. Comparisons between these sets established the neural plate boundary at stages 3d/4. Further analysis categorized graft contributions to anteroposterior and dorsoventral subdivisions of the early neural tube, including data on the floor plate and the eye field. The rostral boundary of the neural plate was contained within the earliest expression domain of the Ganf gene, and the overall shape of the neural plate was contrasted and discussed with regard to the expression patterns of the genes Plato, Sox2, Otx2 and Dlx5 (and others reported in the literature) at stages 3d/4.
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26

Modrell, Melinda S., Dorit Hockman, Benjamin Uy, David Buckley, Tatjana Sauka-Spengler, Marianne E. Bronner, and Clare V. H. Baker. "A fate-map for cranial sensory ganglia in the sea lamprey." Developmental Biology 385, no. 2 (January 2014): 405–16. http://dx.doi.org/10.1016/j.ydbio.2013.10.021.

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27

Dougherty, Max, George Kamel, Valeriy Shubinets, Graham Hickey, Michael Grimaldi, and Eric C. Liao. "Embryonic Fate Map of First Pharyngeal Arch Structures in the sox10." Journal of Craniofacial Surgery 23, no. 5 (September 2012): 1333–37. http://dx.doi.org/10.1097/scs.0b013e318260f20b.

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28

Vicinanza, Carla, Iolanda Aquila, Eleonora Cianflone, Mariangela Scalise, Fabiola Marino, Teresa Mancuso, Francesca Fumagalli, et al. "Kitcre knock-in mice fail to fate-map cardiac stem cells." Nature 555, no. 7697 (March 2018): E1—E5. http://dx.doi.org/10.1038/nature25771.

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29

Spina, Anna, Silviana Rea, Valeria De Pasquale, Vincenzo Mastellone, Luigi Avallone, and Luigi Michele Pavone. "Fate Map of Serotonin Transporter-Expressing Cells in Developing Mouse Thyroid." Anatomical Record: Advances in Integrative Anatomy and Evolutionary Biology 294, no. 3 (February 9, 2011): 384–90. http://dx.doi.org/10.1002/ar.21353.

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30

Pavone, Luigi Michele, Pratibha Mithbaokar, Vincenzo Mastellone, Luigi Avallone, Patricia Gaspar, Veeramani Maharajan, and Antonio Baldini. "Fate map of serotonin transporter-expressing cells in developing mouse heart." genesis 45, no. 11 (2007): 689–95. http://dx.doi.org/10.1002/dvg.20343.

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31

Saint-Jeannet, Jean-Pierre, and Igor R. Dawid. "A Fate Map for the 32-Cell Stage of Rana pipiens." Developmental Biology 166, no. 2 (December 1994): 755–62. http://dx.doi.org/10.1006/dbio.1994.1353.

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32

Bhattacharya, Sudin, Qiang Zhang, and Melvin E. Andersen. "A deterministic map of Waddington's epigenetic landscape for cell fate specification." BMC Systems Biology 5, no. 1 (2011): 85. http://dx.doi.org/10.1186/1752-0509-5-85.

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33

Hatada, Y., and C. D. Stern. "A fate map of the epiblast of the early chick embryo." Development 120, no. 10 (October 1, 1994): 2879–89. http://dx.doi.org/10.1242/dev.120.10.2879.

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We have used carbocyanine dyes (DiI and DiO) to generate fate maps for the epiblast layer of the chick embryo between stage X and the early primitive streak stage (stages 2–3). The overall distribution of presumptive cell types in these maps is similar to that described for other laboratory species (zebrafish, frog, mouse). Our maps also reveal certain patterns of movement for these presumptive areas. Most areas converge towards the midline and then move anteriorly along it. Interestingly, however, some presumptive tissue types do not take part in these predominant movements, but behave in a different way, even if enclosed within an area that does undergo medial convergence and anterior movement. The apparently independent behaviour of certain cell populations suggests that at least some presumptive cell types within the epiblast are already specified at preprimitive streak stages.
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34

Smith, L. J. "Embryonic axis orientation in the mouse and its correlation with blastocyst relationships to the uterus." Development 89, no. 1 (October 1, 1985): 15–35. http://dx.doi.org/10.1242/dev.89.1.15.

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Each of the three primary axes of the primitive streak (6¾ days p.c.) to C-shaped (9½ days) stage mouse embryo has a specific relationship to the uterine horn axes. By a retrograde analysis of younger sectioned embryos it has been possible to construct an axis fate map for the implanting 4¼-day blastocyst and to show how its implantation in one or the other of two specific orientations to the ends and walls of the horn leads to these embryo-horn relationships. The implanting blastocyst axis fate map can be related to an axis fate map of the attached blastocyst (Smith, 1980) since these too are in one or the other of two orientations to the ends and walls of the horn. It is suggested that the asymmetries of the attached and implanting blastocysts that allowed the distinctive attachment and implantation orientations to be recognized, are the initial expressions of a three-dimensional system of positional information that is present in the attached blastocyst.
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35

Tucker, A. S., and J. M. W. Slack. "The Xenopus laevis tail-forming region." Development 121, no. 1 (January 1, 1995): 249–62. http://dx.doi.org/10.1242/dev.121.1.249.

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A fate map is produced for the Xenopus tail-forming region at the neurula stage by orthotopic grafting of tissue labelled with fluorescein-dextran amine. It is shown that the axial tissues of the tail are derived from a rectangle 700 micrometre wide by 600 micrometre long, while the epidermis of the tail is drawn from a much larger area. The fate map shows that much of the final tail is not formed from the tail bud itself, but by a displacement of trunk axial tissue relative to the proctodaeum. A specification map is also produced by culturing parts of the tail-forming region in vitro or as grafts on a neutral site on host embryos. For the axial tissues this map is identical to the fate map, showing that the tail-forming region is embryologically mosaic. The prospective tail epidermis can, however, regulate defects. It is shown that previous claims of regeneration of the Xenopus tail bud are misleading. Removal of the tail-forming region totally prevents tail development. Removal of the tail bud leads to a partial tail, formed by the normal process of displacement of trunk tissue relative to the proctodaeum. Even when only part of the tail bud is removed the tail is still truncated. This shows that there is no terminal regeneration of the tail at embryonic stages.
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36

Ruffins, S. W., and C. A. Ettensohn. "A fate map of the vegetal plate of the sea urchin (Lytechinus variegatus) mesenchyme blastula." Development 122, no. 1 (January 1, 1996): 253–63. http://dx.doi.org/10.1242/dev.122.1.253.

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Previous lineage tracing experiments have shown that the vegetal blastomers of cleavage stage embryos give rise to all the mesoderm and endoderm of the sea urchin larva. In these studies, vegetal blastomers were labeled no later than the sixth cleavage division (60-64 cell stage). In an earlier study we showed that single cells in the vegetal plate of the blastula stage Lytechinus variegatus embryo could be labeled in situ with the fluorescent, lipophilic dye, DiI(C18), and that cells labeled in the central region of the vegetal plate of the mesenchyme blastula primarily gave rise to homogeneous clones consisting of a single secondary mesenchyme cell (SMC) type (Ruffins and Ettensohn (1993) Dev. Biol. 160, 285–288). Our clonal labeling showed that a detailed fate map could be generated using the DiI(C18) labeling technique. Such a fate map could provide information about the spatial relationships between the precursors of specific mesodermal and endodermal cell types and information concerning the movements of these cells during gastrulation and later embryogenesis. We have used this method to construct the first detailed fate map of the vegetal plate of the sea urchin embryo. Ours is a latitudinal map; mapping from the plate center, where the mesodermal precursors reside, through the region which contains the endodermal precursors and across the ectodermal boundary. We found that the precursors of certain SMC types are segregated in the mesenchyme blastula stage vegetal plate and that prospective germ layers reside within specific boundaries. To determine whether the vegetal plate is radially symmetrical with respect to mesodermal cell fates, single blastomeres of four cell stage embryos were injected with lysyl-rhodamine dextran (LRD). The resulting ectodermal labeling patterns were classified and correlated with the SMC types labeled. This analysis indicates that the dorsal and ventral blastomers do not contribute equally to SMC derivatives in L. variegatus.
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37

Grammont, Muriel, and Kenneth D. Irvine. "fringeandNotchspecify polar cell fate duringDrosophilaoogenesis." Development 128, no. 12 (June 15, 2001): 2243–53. http://dx.doi.org/10.1242/dev.128.12.2243.

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fringe encodes a glycosyltransferase that modulates the ability of the Notch receptor to be activated by its ligands. We describe studies of fringe function during early stages of Drosophila oogenesis. Animals mutant for hypomorphic alleles of fringe contain follicles with an incorrect number of germline cells, which are separated by abnormally long and disorganized stalks. Analysis of clones of somatic cells mutant for a null allele of fringe localizes the requirement for fringe in follicle formation to the polar cells, and demonstrates that fringe is required for polar cell fate. Clones of cells mutant for Notch also lack polar cells and the requirement for Notch in follicle formation appears to map to the polar cells. Ectopic expression of fringe or of an activated form of Notch can generate an extra polar cell. Our results indicate that fringe plays a key role in positioning Notch activation during early oogenesis, and establish a function for the polar cells in separating germline cysts into individual follicles.
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38

Hartman, Geoffrey H. "Guest Column: The Fate of Reading Once More." PMLA/Publications of the Modern Language Association of America 111, no. 3 (May 1996): 383–89. http://dx.doi.org/10.1632/s003081290005999x.

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“The fate of reading,” a heavy phrase for which I bear some responsibility, suggests at least a subprophetic talent for anticipating future developments. When things get out of hand, when they seem to speed up, it is tempting to master by very large claims one's panic at being left behind, at becoming obsolete. In literary criticism too, someone redraws the map each year, but new movements quickly become as obsolete as those they displaced.
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39

Lambert, J. D., and L. M. Nagy. "MAPK signaling by the D quadrant embryonic organizer of the mollusc Ilyanassa obsoleta." Development 128, no. 1 (January 1, 2001): 45–56. http://dx.doi.org/10.1242/dev.128.1.45.

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Classical experiments performed on the embryo of the mollusc Ilyanassa obsoleta demonstrate that the 3D macromere acts as an embryonic organizer, by signaling to other cells and inducing them to assume the correct pattern of cell fates. We have discovered that MAP kinase signaling is activated in the cells that require the signal from 3D for normal differentiation. Preventing specification of the D quadrant lineage by removing the polar lobe disrupts the pattern of MAPK activation, as does ablation of the 3D macromere itself. Blocking MAPK activation with the MAP Kinase inhibitor U0126 produces larvae that differentiate the same limited complement of tissues as D quadrant deletions. Our results suggest that the MAP Kinase signaling cascade transduces the inductive signal from 3D and specifies cell fate among the cells that receive the signal.
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40

Matsuzawa, Atsushi, and Hidenori Ichijo. "Redox control of cell fate by MAP kinase: physiological roles of ASK1-MAP kinase pathway in stress signaling." Biochimica et Biophysica Acta (BBA) - General Subjects 1780, no. 11 (November 2008): 1325–36. http://dx.doi.org/10.1016/j.bbagen.2007.12.011.

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41

Guo, Qiuxia, Cynthia Loomis, and Alexandra L. Joyner. "Fate map of mouse ventral limb ectoderm and the apical ectodermal ridge." Developmental Biology 264, no. 1 (December 2003): 166–78. http://dx.doi.org/10.1016/j.ydbio.2003.08.012.

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42

Ezin, Akouavi M., Scott E. Fraser, and Marianne Bronner-Fraser. "Fate map and morphogenesis of presumptive neural crest and dorsal neural tube." Developmental Biology 330, no. 2 (June 2009): 221–36. http://dx.doi.org/10.1016/j.ydbio.2009.03.018.

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43

Vermeer, Jenny A. F., Jonathan Ient, Bostjan Markelc, Jakob Kaeppler, Lydie M. O. Barbeau, Arjan J. Groot, Ruth J. Muschel, and Marc A. Vooijs. "A lineage-tracing tool to map the fate of hypoxic tumour cells." Disease Models & Mechanisms 13, no. 7 (June 22, 2020): dmm044768. http://dx.doi.org/10.1242/dmm.044768.

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ABSTRACTIntratumoural hypoxia is a common characteristic of malignant treatment-resistant cancers. However, hypoxia-modification strategies for the clinic remain elusive. To date, little is known on the behaviour of individual hypoxic tumour cells in their microenvironment. To explore this issue in a spatial and temporally controlled manner, we developed a genetically encoded sensor by fusing the O2-labile hypoxia-inducible factor 1α (HIF-1α) protein to eGFP and a tamoxifen-regulated Cre recombinase. Under normoxic conditions, HIF-1α is degraded but, under hypoxia, the HIF-1α-GFP-Cre-ERT2 fusion protein is stabilised and in the presence of tamoxifen activates a tdTomato reporter gene that is constitutively expressed in hypoxic progeny. We visualise the random distribution of hypoxic tumour cells from hypoxic or necrotic regions and vascularised areas using immunofluorescence and intravital microscopy. Once tdTomato expression is induced, it is stable for at least 4 weeks. Using this system, we could show in vivo that the post-hypoxic cells were more proliferative than non-labelled cells. Our results demonstrate that single-cell lineage tracing of hypoxic tumour cells can allow visualisation of their behaviour in living tumours using intravital microscopy. This tool should prove valuable for the study of dissemination and treatment response of post-hypoxic tumour cells in vivo at single-cell resolution.This article has an associated First Person interview with the joint first authors of the paper.
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44

Helde, K., E. Wilson, C. Cretekos, and D. Grunwald. "Contribution of early cells to the fate map of the zebrafish gastrula." Science 265, no. 5171 (July 22, 1994): 517–20. http://dx.doi.org/10.1126/science.8036493.

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45

Kumano, Gaku, and William C. Smith. "Revisions to theXenopus gastrula fate map: Implications for mesoderm induction and patterning." Developmental Dynamics 225, no. 4 (November 26, 2002): 409–21. http://dx.doi.org/10.1002/dvdy.10177.

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46

Hofmann, D. K., and M. Gottlieb. "Bud formation in the scyphozoan Cassiopea andromeda: epithelial dynamics and fate map." Hydrobiologia 216-217, no. 1 (June 1991): 53–59. http://dx.doi.org/10.1007/bf00026443.

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47

Minsuk, S. B., and R. E. Keller. "Surface mesoderm in Xenopus : a revision of the stage 10 fate map." Development Genes and Evolution 207, no. 6 (December 17, 1997): 389–401. http://dx.doi.org/10.1007/s004270050128.

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48

Woo, K., and S. E. Fraser. "Order and coherence in the fate map of the zebrafish nervous system." Development 121, no. 8 (August 1, 1995): 2595–609. http://dx.doi.org/10.1242/dev.121.8.2595.

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The zebrafish is an excellent vertebrate model for the study of the cellular interactions underlying the patterning and the morphogenesis of the nervous system. Here, we report regional fate maps of the zebrafish anterior nervous system at two key stages of neural development: the beginning (6 hours) and the end (10 hours) of gastrulation. Early in gastrulation, we find that the presumptive neurectoderm displays a predictable organization that reflects the future anteroposterior and dorsoventral order of the central nervous system. The precursors of the major brain subdivisions (forebrain, midbrain, hindbrain, neural retina) occupy discernible, though overlapping, domains within the dorsal blastoderm at 6 hours. As gastrulation proceeds, these domains are rearranged such that the basic order of the neural tube is evident at 10 hours. Furthermore, the anteroposterior and dorsoventral order of the progenitors is refined and becomes aligned with the primary axes of the embryo. Time-lapse video microscopy shows that the rearrangement of blastoderm cells during gastrulation is highly ordered. Cells near the dorsal midline at 6 hours, primarily forebrain progenitors, display anterior-directed migration. Cells more laterally positioned, corresponding to midbrain and hindbrain progenitors, converge at the midline prior to anteriorward migration. These results demonstrate a predictable order in the presumptive neurectoderm, suggesting that patterning interactions may be well underway by early gastrulation. The fate maps provide the basis for further analyses of the specification, induction and patterning of the anterior nervous system, as well as for the interpretation of mutant phenotypes and gene-expression patterns.
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49

Chalmers, A. D., and J. M. Slack. "The Xenopus tadpole gut: fate maps and morphogenetic movements." Development 127, no. 2 (January 15, 2000): 381–92. http://dx.doi.org/10.1242/dev.127.2.381.

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We have produced a comprehensive fate map showing where the organs of the gut and respiratory system are derived from in the early Xenopus laevis endoderm. We also show the origin of the associated smooth muscle layer on a separate fate map. Comparison of the two maps shows that for most organs of the gut the prospective epithelium and smooth muscle do not overlie each other in the early embryo but come together at a later stage. These fate maps should be useful for future studies into endoderm specification. It was not previously known how the elongation of the endoderm occurs, how the single-layered dorsal and many-layered ventral endoderm gives rise to the single layered epithelium, and whether or not the archenteron cavity actually gives rise to the gut lumen. Using a variety of labelling procedures we show firstly, that radial intercalation occurs in the gut transforming a short thick tube into a long thin tube; secondly, that the archenteron lining does not become the definitive gut lumen. Instead the archenteron cavity almost closes at tailbud stages before providing a nucleus for the definitive gut cavity, which opens up during elongation. Based on this work we present a model explaining the morphogenesis of the gut.
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50

Furner, I. J., J. F. Ainscough, J. A. Pumfrey, and L. M. Petty. "Clonal analysis of the late flowering fca mutant of Arabidopsis thaliana: cell fate and cell autonomy." Development 122, no. 3 (March 1, 1996): 1041–50. http://dx.doi.org/10.1242/dev.122.3.1041.

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Plants that are homozygous for the fca mutation bolt and flower later than wild-type (FCA) plants. The mutation has little or no effect on the fate map of the dry seed, except that the central cells give rise to further rosette leaves instead of the bolting stem, cauling leaves and inflorescence. The large and variable sectors affecting the late rosette leaves of fca plants were used to generate an abstract frequency-distance fate map of vegetative growth. The map relates the initiation of leaves in the plant apex to their final arrangements. The map was found to be a shallow dome with phyllotaxy superimposed on its surface. X-irradiation was used to provoke loss of the FCA allele from cells in heterozygous seeds. The resulting fca sectors had no effect on the plant phenotype. Even when L2 and L3 cells at the centre of the meristem could not produce the FCA gene product, bolting and flowering was unaffected. The genotypically fca mutant tissue was incorporated into phenotypically normal stems, cauline leaves and flowers. Possible reasons for the non-autonomous behaviour of the trait are discussed.
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