1 re ischemia reperfusion injury (genetic cell
fate mapping).
2 Tribolium embryos with wild-type and altered
fate maps.
3 cing for antibody lineage tracing and B cell
fate mapping.
4 he epicardium, epicardial-derived cells, and
fate mapping.
5 gesting that Sox2-CreER may not be useful to
fate map a supporting cell origin of regenerated hair ce
6 itional, inducible transgenic mouse model to
fate map adult-generated DGCs.
7 ng injury and an SPC-driven inducible cre to
fate-map AECs, we found the majority of type II AECs in
8 Our mRNA expression and
fate mapping analyses demonstrate that the dorsolateral
9 Surprisingly, however, genotyping and
fate mapping analyses reveal that chondrocytes constitut
10 endocardial cell-specific Cre mouse line for
fate-mapping analyses of valve endocardial cells.
11 Mouse genetic
fate-mapping analyses show that embryonically, a c-Kit(+
12 Fate mapping analysis showed that IL-17-expressing exFox
13 electroencephalography/video-monitoring, and
fate mapping analysis.
14 Genetic
fate-mapping analysis confirms that the newly formed myo
15 Our intersectional
fate-mapping analysis further reveals that Emx1-lineage
16 Furthermore, genetic
fate-mapping analysis suggests that subpial precursors c
17 ltiple genetically engineered mice to track,
fate map and ablate cells to determine the source and fu
18 Using genetic tools to
fate map and manipulate a cranial mesenchymal progenitor
19 We used
fate mapping and AID(GFP) reporter mice to determine if
20 Fate mapping and cell lineage tracing studies have recen
21 Fate mapping and chimera studies, however, failed to pro
22 Genetic
fate mapping and clonal analysis of individual cells rev
23 Eight weeks post MI,
fate mapping and flow cytometry revealed that a 2.9-fold
24 Using in vivo
fate mapping and flow cytometry, we estimated that durin
25 ination of in vitro explant culture, genetic
fate mapping and gene overexpression and knockdown to ex
26 Cell-
fate mapping and gene-deletion studies using zG-specific
27 Current
fate mapping and imaging platforms are limited in their
28 Using in vivo genetic
fate mapping and in vitro clonal analysis, we identified
29 Concurrent
fate mapping and labeling with mitotic tracers showed th
30 Using photoconversion-based
fate mapping and live cell tracking coupled with laser a
31 Genetic
fate mapping and loss of function studies in mice demons
32 Fate mapping and microdissection experiments have demons
33 these unresolved questions, with emphasis on
fate mapping and modeling of the hematopoietic flow from
34 Using
fate mapping and mutant analysis, we find that PAA proge
35 Genetic
fate mapping and neurochemical profile demonstrate that
36 Using genetic
fate mapping and orthotopic transplantation, we provide
37 Combining single-cell
fate mapping and three-dimensional cell tracking in the
38 ences contribute to fidelity of phylogenetic
fate maps and to explore statistical methods for assessi
39 rain circuits using a combination of genetic
fate-mapping and assays in mice.
40 Marker analysis as well as
fate-mapping and chimera studies demonstrate for the fir
41 Through genetic
fate-mapping and conditional ablation, we provide eviden
42 Two recent studies use
fate-mapping and limiting dilution transplantation assay
43 We used
fate-mapping and other methods to demonstrate that utric
44 Fate-mapping and single-cell RNA sequencing studies also
45 al4-UAS binary expression, Cre-loxP-mediated
fate-mapping and the establishment of novel, tissue-spec
46 Il17a
fate-mapping and transcriptional profiling provide evide
47 tes to the atrium in zebrafish by multicolor
fate-mapping and we compare our analysis to the establis
48 anner predicted from classical developmental
fate mapping,
and differentiate into each of the three p
49 lizing a combination of genetics, retroviral
fate mapping,
and lineage-specific retroviral barcode la
50 Here, using an inducible Cre-lox
fate mapping approach with the ShhcreER(T2) mouse line,
51 We have taken a genetic-based
fate-mapping approach to determine the specific contribu
52 We used an inducible, Cre-loxP in vivo
fate-mapping approach to examine the contributions of th
53 Using a novel
fate-mapping approach, we demonstrate that precursors in
54 Here, we addressed this issue using a Treg
fate-mapping approach, which revealed that Treg loss was
55 METHODS AND Using 2 in vivo
fate-mapping approaches combined with a smooth muscle ce
56 Using 2 in vivo
fate-mapping approaches combined with a smooth muscle ce
57 However, using parabiosis and
fate-mapping approaches in mice, we found that CNS macro
58 ave investigated this question using genetic
fate-mapping approaches in mice.
59 we use loss-of-function, label-retention and
fate-mapping approaches in the little skate to demonstra
60 Using high-resolution genetic
fate-mapping approaches with cKit(CreERT2/+) and Wnt1::F
61 Using new genetic
fate-mapping approaches, here we identify a population o
62 Using parabiosis and
fate-mapping approaches, we confirmed that monocytes do
63 Using multiple
fate-mapping approaches, we show that arterial macrophag
64 Using murine models of atherosclerosis and
fate-mapping approaches, we show that hematopoietic stem
65 ent advances in genetic lineage analysis and
fate mapping are facilitating such studies.
66 Nestin
fate-mapped astrocytes also flow anteriorly from the SVZ
67 Fate mapping at multiple time points in combination with
68 Fate mapping at the open neural plate stage was carried
69 We generated a Bapx1(Cre) knock-in allele to
fate map Bapx1-expressing cells and evaluate its functio
70 ay toward construction of retrospective cell-
fate maps based on mutations accumulating in genomes of
71 cing systems are not suitable for epicardial
fate mapping because of endogenous endothelial expressio
72 Combining genetic
fate-mapping,
birth-dating, and gene expression studies,
73 Genetic
fate-mapping by means of an inducible Cre-LoxP recombina
74 ing cardiomyocytes, and suggest that hypoxia
fate mapping can be a powerful tool for identifying cycl
75 combination of approaches, including genetic
fate mapping,
cell birth dating, cell migration assays,
76 We show here by
fate mapping,
clonal analysis, and immunohistochemistry
77 To this end, we established multicongenic
fate mapping combined with mathematical modeling to quan
78 f the cardiogenic mesoderm based on this new
fate map confirmed these results and, in addition, showe
79 Fate mapping confirmed that in the course of mesial temp
80 Inducible genetic
fate mapping confirmed that new bone cells do not arise
81 Inducible genetic
fate mapping conveniently allows for the labeling of EBG
82 These nestin
fate-mapped corpus callosum astrocytes are uniformly pos
83 Fate-mapped cortical GFAP(+) cells derived ex vivo from
84 x3(Cre/+) and Hoxb1(Cre/+) mice to label and
fate map cranial NEC lineages, we have demonstrated that
85 In addition, these
fate mapping data indicate that renal development, like
86 n vivo, and reconcile conflicting positional
fate mapping data regarding the primary heart-forming fi
87 y-finned fish Polyodon spathula, and present
fate-mapping data that conclusively demonstrate a latera
88 In contrast to murine
fate-mapping data, which indicate that only ILC3s expres
89 Time-lapse imaging and
fate mapping demonstrate that the dorsal habenulae (dHb)
90 erior pituitary and, using genetic inducible
fate mapping,
demonstrate that they serve to generate su
91 Genetic
fate mapping demonstrated that cMPhi derived from CX3CR1
92 Inducible
fate mapping demonstrates that BMI1 is expressed in vivo
93 The
fate mapped E11.5-12.5 STN neuronal population included
94 nce of multipotent NSCs, as shown by in vivo
fate mapping experiments in the adult subependymal zone
95 Fate mapping experiments revealed a contribution of the
96 However, genetic
fate mapping experiments suggest that mesenchyme-derived
97 ment using a number of assays, including Cre-
fate mapping experiments.
98 Fate-mapping experiments demonstrated that neighboring s
99 Our
fate-mapping experiments identify, in the fetal liver, a
100 Importantly,
fate-mapping experiments revealed that ESCs commonly ari
101 Moreover,
fate-mapping experiments revealed that the timing of SOX
102 Fate-mapping experiments showed that outside the most an
103 was distal from the DC lineage, as shown by
fate-mapping experiments using Zbtb46.
104 e of these cells has not been proven through
fate-mapping experiments.
105 Moreover, dSPNs, as marked by Isl1-cre
fate map,
express Sox8 in the embryonic striatum and Sox
106 ee legs differ in their morphology, only the
fate map for the T1 (prothoracic) leg disc has been gene
107 Here we present
fate maps for the T2 (meso-) and T3 (metathoracic) leg d
108 field and its myocardial component has been
fate mapped from the epiblast to the heart in both mamma
109 aexpression patterns, PP are comparable to a
fate map generated experimentally by laser ablation and
110 First, genetic inducible
fate mapping (
GIFM) with an Ascl1(CreER) allele was foun
111 f adult MbDA neurons using genetic inducible
fate mapping (
GIFM).
112 hip between monocyte subsets was verified by
fate mapping grafted human classical monocytes into huma
113 Fate mapping has shown that mature tissues such as blood
114 Using inducible genetic
fate mapping,
here we examined the developmental fate of
115 Fate mapping,
however, reveals that intermediate cells r
116 aneously beating myocytes in vitro; cre/LoxP
fate mapping identified a noncardiac population of (c-ki
117 Using genetic
fate mapping in mice, we show that in the absence of Ptf
118 Clonal
fate mapping in vivo reveals heterogeneity in Ascl1-expr
119 t permit both prospective identification and
fate mapping in vivo.
120 ification of IL-22-producing cells and their
fate mapping in vivo.
121 Using genetic
fate mapping in wild-type and Lmx1a(-/-) mice, we demons
122 c changes and establishing cell lineages and
fate maps in vivo.
123 dney cells expressing renin were genetically
fate-mapped in adult Ren1cCreERxRs-tdTomato-R, Ren1cCrex
124 deficient mutants in zebrafish, and physical
fate-mapping in frog and lamprey, we find that NECs are
125 Using genetic
fate-mapping in the mouse, we found that the epithelial
126 we present the first detailed spatiotemporal
fate-maps in any vertebrate for the ophthalmic trigemina
127 in mice from Wnt1Cre and Atoh1 CreER lineage
fate mapping,
in common with the major precerebellar nuc
128 Genetic
fate mapping indicated that the majority of cardiomyocyt
129 g loss-of-function experiments and inducible
fate-mapping,
indicated that nNOS(+) IvCs and NGCs are b
130 A-based strains, SMA-Cre(ERT2) and SMA-rtTA,
fate mapped into the majority of cold-induced beige adip
131 nitors are also highly labeled when Flt3-Cre
fate mapping is applied.
132 However, a problem with such "phylogenetic
fate maps"
is that they cannot be verified experimentall
133 roposterior (AP) origin of the IP complex by
fate-mapping its neuromeric origin in the chick, discove
134 Using NFIL3-deficient mice, PLZF reporter/
fate mapping mice, and mixed bone marrow chimeras, we id
135 meric animals and Foxp3-GFP/ERT2-Cre/dTomato
fate-mapping mice show that TLR-initiated DC autocrine C
136 In this study,
fate-mapping mice were used to assess the stability of T
137 ed in culture with CD4(+) T cells from Il17a
fate-mapping mice, were adoptively transferred to assess
138 Using a genetic
fate-mapping model that allows us to trace the progeny o
139 We developed a
fate-mapping model where cells with a history of RAG-1 e
140 Using
fate-mapping models and monocytopenic mice, together wit
141 To investigate this, we performed targeted
fate-mapping,
molecular characterisation and cell cycle
142 Recently, using a bi-transgenic ACM
fate mapping mouse model and an in vitro culture system,
143 Here we used two new
fate-mapping mouse models to track Th17 cells during imm
144 Here we combine intersectional
fate mapping,
neuron sorting, and genome-wide RNA-seq to
145 ux2 expression pattern, the vast majority of
fate-mapped neurons express Satb2 but not Ctip2, confirm
146 of cell growth, as was used to construct the
fate map of Caenorhabditis elegans, but is not possible
147 n and thus allows us to propose a prosomeric
fate map of GABAergic cell populations.
148 des the first overview of the spatiotemporal
fate map of Neurog1 lineages in the CNS.
149 ometry of the early cleavage pattern and the
fate map of the blastula, along with similarities in lar
150 dings provide a complete and high-resolution
fate map of the Drosophila appendage primordia, linking
151 e tools to generate a comprehensive regional
fate map of the mouse subpallium, including sources for
152 We have generated a
fate map of the otic placode and show that precursors fo
153 llowed us to define a comprehensive regional
fate map of the pallium.
154 Utilizing the published
fate map of the spiral-cleaving annelid Capitella teleta
155 NMR-based quantitative
fate mapping of (13)C-labeled substrates revealed that l
156 We performed in vivo
fate mapping of adult hair follicle dermal sheath (DS) c
157 of individual memory lymphocytes by in vivo
fate mapping of CD8(+) T cells and their descendants acr
158 Fate mapping of chick tailbud further revealed that spre
159 These studies provide an in vivo model for
fate mapping of DCs, distinguishing them from other leuk
160 Using inducible genetic
fate mapping of Dlx1/2 precursors, we analyzed the produ
161 Here we report
fate mapping of hypoxic cells and their progenies by gen
162 In addition,
fate mapping of mouse neurons made from the same pool of
163 Fate mapping of nestin(+) cells unambiguously revealed t
164 stigations in quail-chick chimeras involving
fate mapping of neural crest cells to the ultimobranchia
165 Fate mapping of neural crest-derived tissues indicates t
166 rough systematic targeting of cell types and
fate mapping of neural progenitors.
167 NG2 cell fate determination, we used genetic
fate mapping of NG2 cells in constitutive and tamoxifen-
168 nic transcription factor drivers allow finer
fate mapping of progenitor pools that give rise to disti
169 Clonal analysis and
fate mapping of single, identified cells show that trach
170 egeneration in the postnatal cochlea rely on
fate mapping of supporting cells.
171 However,
fate mapping of these cycling cardiomyocytes has not bee
172 Fate maps of different discs have been generated that sh
173 are able to track cell lineages, to generate
fate maps of the blastema and to identify the progenitor
174 Genetic
fate-mapping of Alpi(+) cells before or during targeted
175 ion and gut vascular development we combined
fate-mapping of ENCC with immunolabelling and intravascu
176 Cre recombinase-based, genetic
fate-mapping of larval or adult tcf21(+) cells revealed
177 using an in utero MF-depletion strategy and
fate-mapping of yolk sac (YS) and fetal liver (FL) hemat
178 and DiO labelling to produce eight detailed
fate-maps of chick embryonic head ectoderm over approxim
179 r, these results constitute a comprehensive "
fate map"
of replication-timing changes during early mou
180 a functional analysis, using CRISPR/Cas9 and
fate mapping,
of 5' hox genes and enhancers in zebrafish
181 We utilized a combination of genetic
fate mapping,
parabiotic, transcriptional, and functiona
182 ssessed the cellular origin of new myelin by
fate mapping platelet-derived growth factor receptor alp
183 We addressed this issue by
fate mapping Plp-Cre-ER(T2)/Rosa26-EYFP (PCE/R) double-t
184 Although intestinal Rorc
fate map-
positive (Rorc(fm+)) ILCs show a clear ILC3 phe
185 urrently in use by several investigators for
fate mapping purposes, and may be adopted by others in t
186 ationships between cells in the phylogenetic
fate map reflect biological information regarding the or
187 Ventricular contractile function and the VCS
fate map remained unchanged in VCS-specific Tbx5 knockou
188 Cre/Lox techniques to genetically label and
fate map renal epithelia in models of kidney fibrosis.
189 Analysis with Treg
fate-mapping reporter mice further demonstrates that IL-
190 Thus, our novel dynamic positional
fate maps resolve the origin of cardiac progenitor cells
191 onent of the exocrine pancreas; however, our
fate-mapping results indicate that CACs are more closely
192 Our genetic
fate-mapping results show that Isl1-expressing progenito
193 on including expression of NEUROG1, although
fate-mapping results suggest SOX2 may be required as a c
194 ng regions of the orofacial prominences that
fate mapping revealed contribute to the upper lip and pr
195 Fate mapping revealed that a fraction of Treg cells lost
196 Furthermore, long-term genetic
fate mapping revealed that TrkB deletion severely compro
197 Genetic
fate mapping revealed that yolk-sac and fetal monocyte p
198 However, Cre-lox-based genetic
fate-mapping revealed a small subpopulation of myenteric
199 Fate mapping reveals that >90% of adult oligodendrocytes
200 Fate mapping reveals that the new population derives lar
201 Fate maps show that polarizing region and adjacent cells
202 Fate-mapping showed that LepR(+) cells arose postnatally
203 Here, we performed genetic
fate mapping,
showing that VGLUT3 lineage sensory neuron
204 Cre-Lox
fate mapping shows this region gives rise to inner hair
205 e and describe animal models to identify and
fate-map stem and progenitor cells expressing each Notch
206 e-driven mouse mammary tumor models and cell-
fate mapping strategies, we show in vivo evidence for th
207 of fluorescent reporter transgenes, genetic
fate-mapping strategies and a ventricle-specific genetic
208 is proposal by using a genetic knock-in cell
fate mapping strategy in different murine SCI models.
209 By combining an inducible genetic
fate mapping strategy with electrophysiological analysis
210 Using a Cre/loxP genetic
fate mapping strategy, we demonstrate that Six1-positive
211 Prior reports that used a reporter gene
fate-mapping strategy are limited in their ability to in
212 We developed an in vivo
fate-mapping strategy that enabled us to follow OSN matu
213 Using genetic mouse models and a
fate-mapping strategy, we determined that vascular peric
214 pporting cells demonstrating its utility for
fate mapping studies beyond this age.
215 Recent genetic
fate mapping studies demonstrated that recovery from AKI
216 oughout development, consistent with genetic
fate mapping studies demonstrating that Rax+ lineages gi
217 Fate mapping studies following transient expression of P
218 Genetic inducible
fate mapping studies have identified two principal epith
219 ne fetal and adult hematopoiesis, while cell-
fate mapping studies have revealed complex developmental
220 We identified Ebf2, through
fate mapping studies, as a novel marker for cortical hem
221 Based on our Genetic Inducible
Fate Mapping studies, we propose a model where SHH signa
222 Recent
fate-mapping studies and gene-expression profiles sugges
223 Recent
fate-mapping studies concluded that EMT is not required
224 New genetic
fate-mapping studies have identified pericytes and the c
225 Fate-mapping studies of the Sox9(+) domain revealed endo
226 Furthermore, clonal analysis in NSC
fate-mapping studies revealed a previously unknown role
227 Genetic
fate-mapping studies revealed that the ER71-expressing c
228 Previously reported Cre-based
fate-mapping studies showed that Isl1 progenitors contri
229 Genetic
fate-mapping studies suggest minimal contribution; howev
230 ope has been subdued recently by a series of
fate-mapping studies that cast NG2-glia as dedicated oli
231 Whilst recent genetic
fate-mapping studies using lineage-specific promoters ha
232 reporters after Cre recombination allow for
fate-mapping studies when used in combination with appro
233 Previously published
fate-mapping studies, extended here, show that 3a and 3b
234 In
fate-mapping studies, FITC-labeled vertebra periosteal c
235 Using high-resolution genetic analyses and
fate-mapping studies, three main mononuclear phagocyte l
236 deposition during fibrosis based largely on
fate-mapping studies.
237 s by undertaking the first long-term in vivo
fate-mapping study in any cartilaginous fish.
238 A
fate-mapping study revealed that Tsc1-null Tregs that lo
239 cial to the morphogenesis of the head, which
fate maps suggest arises primarily from the disc proper,
240 d 4 was recently given support by short-term
fate maps,
suggesting that the chick wing polarizing reg
241 ere, we present a new multicolor fluorescent
fate mapping system and quantification approach to inves
242 e we establish a new multicolor fluorescence
fate mapping system to monitor microglial dynamics durin
243 demonstrate the general utility of our novel
fate-mapping system to follow cell population dynamics i
244 We used an intersectional
fate-mapping system using the RC::FrePe allele, which re
245 Herein, we used various multicolor
fate mapping systems to investigate the ontogeny and dyn
246 Genetic
fate mapping tagged 41.4+/-4.1% of the cardiac adipocyte
247 In contrast to previously
fate-mapped Tbx18/WT-1-expressing cells that give rise t
248 Here we use a novel genetic
fate mapping technique to simultaneously track multiple
249 Here, using genetic
fate map techniques, we demonstrate that cardiac fibrobl
250 The combination of inducible genetic
fate mapping techniques with in vitro targeted patch-cla
251 eveloping chick embryo using two independent
fate mapping techniques.
252 Using
fate-mapping techniques, we demonstrate that the princip
253 Here, we show by inducible genetic
fate mapping that type I collagen-producing submesotheli
254 Here we show using long-term
fate maps that Green fluorescent protein-expressing chic
255 We present vital dye
fate maps that suggest the somatopleure is eliminated in
256 Here we show, using clonal genetic
fate mapping,
that Mesp1+ cells in gastrulating mesoderm
257 We have
fate mapped the dental mesenchyme, using in vitro tissue
258 Fate-mapping the headfold-stage (~7.75-8.0 dpc) posterio
259 en studied by marker expression analysis and
fate-mapping,
the mechanisms that control the progressio
260 We
fate-map this mesoderm in the axolotl (Ambystoma mexican
261 In vivo
fate mapping through T-cell receptor sequencing allowed
262 e next employed inducible lineage tracing to
fate map,
through Cre recombinase-mediated fluorescent r
263 gene expression in pallial protodomains that
fate map to distinct cortical regions.
264 We used in vivo genetic
fate mapping to assess the behavior of each progenitor t
265 Here, we used genetic
fate mapping to chart the embryological origins of the t
266 Here, we utilize in vivo genetic
fate mapping to demonstrate that Fezf2-expressing radial
267 Here, we use genetic
fate mapping to demonstrate that spontaneous myelin repa
268 In this report, we use molecular
fate mapping to demonstrate that the majority of cell ty
269 Here, we use genetic
fate mapping to examine the progeny of GFAP(+) cells aft
270 We now report on using Cre-based
fate mapping to indelibly label pancreatic Notch-respons
271 Using Genetic Inducible
Fate Mapping to mark adult Gli1- or Smooth muscle actin-
272 Using genetic inducible
fate mapping to mark the Sonic hedgehog (Shh) and Gli1 l
273 we use in utero electroporation and genetic
fate mapping to show that SNPs and RGCs cohabit the VZ b
274 Here, we used genetic
fate mapping to show that Tlx3(+) spinal cord neurons an
275 Surprisingly, static
fate maps together with dynamic confocal imaging reveal
276 ed, hindered by a dearth of genetic tools to
fate map,
track and manipulate beige progenitors and 'be
277 We show by genetic inducible
fate mapping using a Gbx2(CreER) knock-in mouse line tha
278 c eminence and dorsal preoptic area based on
fate mapping using an Shh-Cre allele.
279 Fate mapping using BrdU pulse-chase experiments revealed
280 We perform long-term
fate mapping using GFP-transgenic axolotl and Xenopus la
281 nducted Ascl1- and Ngn2-inducible expression
fate mapping using the CreER/LoxP system.
282 By
fate mapping vz-derived cells in Ascl1 mutants, we furth
283 Using genetic
fate mapping,
we demonstrate here that the majority of c
284 ilizing simultaneous dual and intersectional
fate mapping,
we demonstrate that this boundary is preci
285 Using genetic
fate mapping,
we found that median eminence tanycytes ge
286 Using conditional genetics and
fate mapping,
we show that Notch signaling is essential
287 Kaede protein as well as Cre-driven genetic
fate mapping,
we show that osteoblasts migrate to the si
288 Using inducible genetic
fate mapping,
we show that the individual involvement of
289 Here, by using genetic
fate-mapping,
we demonstrate that new corpus callosum as
290 Through
fate-mapping,
we find that Hh signaling is required at e
291 us-specific Treg cells combined with genetic
fate-mapping,
we noted that a majority of the Treg cells
292 Here we demonstrate the use of
fate mapping wherein microglia and monocyte-derived cell
293 , we generate retina, RPE and lens subdomain
fate maps,
which reveal novel adjacencies that might det
294 g system that combines Cre/lox-assisted cell
fate mapping with a thymidine kinase (sr39tk) reporter g
295 Genetic
fate mapping with an inducible Casz1 allele demonstrates
296 Using genetic inducible
fate mapping with Gli1(CreERT2), we marked Hh-receiving
297 Here, we combined genetic
fate mapping with highly efficient podocyte isolation pr
298 hly mitotic and short-lived in vivo based on
fate-mapping with Ascl1(CreERT2) and Dlx1(CreERT2).
299 Using genetic
fate-mapping with Cux2-Cre and Cux2-CreERT2 mice we demo
300 wo different pulse-chase approaches--genetic
fate-mapping with stable isotope labelling, and multi-is