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FIG. 8. Model describing the role of Notch signaling and <t>Jag1-Notch</t> interaction in zebrafish thyroid development. The thyroid primordium originates from the pharyngeal endoderm by 24 hpf. Our data indicate that Notch signaling originating from the endodermal layer itself or from the surrounding developing tissues plays a fundamental role in limiting the number of thyroidal differentiating precursors (double dotted arrow, 1, left side of the panel). The combined expression of nkx2.1a, pax2a, hhex, and pax8 is distinctive of the thyroid follicular cells. jag1b is mainly expressed starting from at 48 hpf; nevertheless, we can not completely exclude jag1b contribution in earlier phases of thyroid development (“jag1b?”), due to its spotted pattern of expression in the region of the thyroid primordium origin at 24 hpf; jag1a is mainly expressed at 72 hpf, in the most anterior portion of the first thyroid follicle. By 72 hpf, the thyroid tissue starts to elongate posteriorly and produce T4. Jag1-Notch signaling sustains these steps and the maintenance of thyroid cells (dotted black arrow, 2). jag1 loss-of- function conditions impair thyroid development and function (black arrow, 3). T, Thyroid; ch, ceratohyal; h, heart. Stages, upper part of the panel; 24 and 36 hpf, transversal views; from 48 to 120 hpf, ventral views.
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FIG. 8. Model describing the role of Notch signaling and <t>Jag1-Notch</t> interaction in zebrafish thyroid development. The thyroid primordium originates from the pharyngeal endoderm by 24 hpf. Our data indicate that Notch signaling originating from the endodermal layer itself or from the surrounding developing tissues plays a fundamental role in limiting the number of thyroidal differentiating precursors (double dotted arrow, 1, left side of the panel). The combined expression of nkx2.1a, pax2a, hhex, and pax8 is distinctive of the thyroid follicular cells. jag1b is mainly expressed starting from at 48 hpf; nevertheless, we can not completely exclude jag1b contribution in earlier phases of thyroid development (“jag1b?”), due to its spotted pattern of expression in the region of the thyroid primordium origin at 24 hpf; jag1a is mainly expressed at 72 hpf, in the most anterior portion of the first thyroid follicle. By 72 hpf, the thyroid tissue starts to elongate posteriorly and produce T4. Jag1-Notch signaling sustains these steps and the maintenance of thyroid cells (dotted black arrow, 2). jag1 loss-of- function conditions impair thyroid development and function (black arrow, 3). T, Thyroid; ch, ceratohyal; h, heart. Stages, upper part of the panel; 24 and 36 hpf, transversal views; from 48 to 120 hpf, ventral views.
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FIG. 8. Model describing the role of Notch signaling and <t>Jag1-Notch</t> interaction in zebrafish thyroid development. The thyroid primordium originates from the pharyngeal endoderm by 24 hpf. Our data indicate that Notch signaling originating from the endodermal layer itself or from the surrounding developing tissues plays a fundamental role in limiting the number of thyroidal differentiating precursors (double dotted arrow, 1, left side of the panel). The combined expression of nkx2.1a, pax2a, hhex, and pax8 is distinctive of the thyroid follicular cells. jag1b is mainly expressed starting from at 48 hpf; nevertheless, we can not completely exclude jag1b contribution in earlier phases of thyroid development (“jag1b?”), due to its spotted pattern of expression in the region of the thyroid primordium origin at 24 hpf; jag1a is mainly expressed at 72 hpf, in the most anterior portion of the first thyroid follicle. By 72 hpf, the thyroid tissue starts to elongate posteriorly and produce T4. Jag1-Notch signaling sustains these steps and the maintenance of thyroid cells (dotted black arrow, 2). jag1 loss-of- function conditions impair thyroid development and function (black arrow, 3). T, Thyroid; ch, ceratohyal; h, heart. Stages, upper part of the panel; 24 and 36 hpf, transversal views; from 48 to 120 hpf, ventral views.
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FIG. 8. Model describing the role of Notch signaling and <t>Jag1-Notch</t> interaction in zebrafish thyroid development. The thyroid primordium originates from the pharyngeal endoderm by 24 hpf. Our data indicate that Notch signaling originating from the endodermal layer itself or from the surrounding developing tissues plays a fundamental role in limiting the number of thyroidal differentiating precursors (double dotted arrow, 1, left side of the panel). The combined expression of nkx2.1a, pax2a, hhex, and pax8 is distinctive of the thyroid follicular cells. jag1b is mainly expressed starting from at 48 hpf; nevertheless, we can not completely exclude jag1b contribution in earlier phases of thyroid development (“jag1b?”), due to its spotted pattern of expression in the region of the thyroid primordium origin at 24 hpf; jag1a is mainly expressed at 72 hpf, in the most anterior portion of the first thyroid follicle. By 72 hpf, the thyroid tissue starts to elongate posteriorly and produce T4. Jag1-Notch signaling sustains these steps and the maintenance of thyroid cells (dotted black arrow, 2). jag1 loss-of- function conditions impair thyroid development and function (black arrow, 3). T, Thyroid; ch, ceratohyal; h, heart. Stages, upper part of the panel; 24 and 36 hpf, transversal views; from 48 to 120 hpf, ventral views.
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FIG. 8. Model describing the role of Notch signaling and <t>Jag1-Notch</t> interaction in zebrafish thyroid development. The thyroid primordium originates from the pharyngeal endoderm by 24 hpf. Our data indicate that Notch signaling originating from the endodermal layer itself or from the surrounding developing tissues plays a fundamental role in limiting the number of thyroidal differentiating precursors (double dotted arrow, 1, left side of the panel). The combined expression of nkx2.1a, pax2a, hhex, and pax8 is distinctive of the thyroid follicular cells. jag1b is mainly expressed starting from at 48 hpf; nevertheless, we can not completely exclude jag1b contribution in earlier phases of thyroid development (“jag1b?”), due to its spotted pattern of expression in the region of the thyroid primordium origin at 24 hpf; jag1a is mainly expressed at 72 hpf, in the most anterior portion of the first thyroid follicle. By 72 hpf, the thyroid tissue starts to elongate posteriorly and produce T4. Jag1-Notch signaling sustains these steps and the maintenance of thyroid cells (dotted black arrow, 2). jag1 loss-of- function conditions impair thyroid development and function (black arrow, 3). T, Thyroid; ch, ceratohyal; h, heart. Stages, upper part of the panel; 24 and 36 hpf, transversal views; from 48 to 120 hpf, ventral views.
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FIG. 8. Model describing the role of Notch signaling and <t>Jag1-Notch</t> interaction in zebrafish thyroid development. The thyroid primordium originates from the pharyngeal endoderm by 24 hpf. Our data indicate that Notch signaling originating from the endodermal layer itself or from the surrounding developing tissues plays a fundamental role in limiting the number of thyroidal differentiating precursors (double dotted arrow, 1, left side of the panel). The combined expression of nkx2.1a, pax2a, hhex, and pax8 is distinctive of the thyroid follicular cells. jag1b is mainly expressed starting from at 48 hpf; nevertheless, we can not completely exclude jag1b contribution in earlier phases of thyroid development (“jag1b?”), due to its spotted pattern of expression in the region of the thyroid primordium origin at 24 hpf; jag1a is mainly expressed at 72 hpf, in the most anterior portion of the first thyroid follicle. By 72 hpf, the thyroid tissue starts to elongate posteriorly and produce T4. Jag1-Notch signaling sustains these steps and the maintenance of thyroid cells (dotted black arrow, 2). jag1 loss-of- function conditions impair thyroid development and function (black arrow, 3). T, Thyroid; ch, ceratohyal; h, heart. Stages, upper part of the panel; 24 and 36 hpf, transversal views; from 48 to 120 hpf, ventral views.
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FIG. 8. Model describing the role of Notch signaling and <t>Jag1-Notch</t> interaction in zebrafish thyroid development. The thyroid primordium originates from the pharyngeal endoderm by 24 hpf. Our data indicate that Notch signaling originating from the endodermal layer itself or from the surrounding developing tissues plays a fundamental role in limiting the number of thyroidal differentiating precursors (double dotted arrow, 1, left side of the panel). The combined expression of nkx2.1a, pax2a, hhex, and pax8 is distinctive of the thyroid follicular cells. jag1b is mainly expressed starting from at 48 hpf; nevertheless, we can not completely exclude jag1b contribution in earlier phases of thyroid development (“jag1b?”), due to its spotted pattern of expression in the region of the thyroid primordium origin at 24 hpf; jag1a is mainly expressed at 72 hpf, in the most anterior portion of the first thyroid follicle. By 72 hpf, the thyroid tissue starts to elongate posteriorly and produce T4. Jag1-Notch signaling sustains these steps and the maintenance of thyroid cells (dotted black arrow, 2). jag1 loss-of- function conditions impair thyroid development and function (black arrow, 3). T, Thyroid; ch, ceratohyal; h, heart. Stages, upper part of the panel; 24 and 36 hpf, transversal views; from 48 to 120 hpf, ventral views.
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FIG. 8. Model describing the role of Notch signaling and <t>Jag1-Notch</t> interaction in zebrafish thyroid development. The thyroid primordium originates from the pharyngeal endoderm by 24 hpf. Our data indicate that Notch signaling originating from the endodermal layer itself or from the surrounding developing tissues plays a fundamental role in limiting the number of thyroidal differentiating precursors (double dotted arrow, 1, left side of the panel). The combined expression of nkx2.1a, pax2a, hhex, and pax8 is distinctive of the thyroid follicular cells. jag1b is mainly expressed starting from at 48 hpf; nevertheless, we can not completely exclude jag1b contribution in earlier phases of thyroid development (“jag1b?”), due to its spotted pattern of expression in the region of the thyroid primordium origin at 24 hpf; jag1a is mainly expressed at 72 hpf, in the most anterior portion of the first thyroid follicle. By 72 hpf, the thyroid tissue starts to elongate posteriorly and produce T4. Jag1-Notch signaling sustains these steps and the maintenance of thyroid cells (dotted black arrow, 2). jag1 loss-of- function conditions impair thyroid development and function (black arrow, 3). T, Thyroid; ch, ceratohyal; h, heart. Stages, upper part of the panel; 24 and 36 hpf, transversal views; from 48 to 120 hpf, ventral views.
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FIG. 8. Model describing the role of Notch signaling and <t>Jag1-Notch</t> interaction in zebrafish thyroid development. The thyroid primordium originates from the pharyngeal endoderm by 24 hpf. Our data indicate that Notch signaling originating from the endodermal layer itself or from the surrounding developing tissues plays a fundamental role in limiting the number of thyroidal differentiating precursors (double dotted arrow, 1, left side of the panel). The combined expression of nkx2.1a, pax2a, hhex, and pax8 is distinctive of the thyroid follicular cells. jag1b is mainly expressed starting from at 48 hpf; nevertheless, we can not completely exclude jag1b contribution in earlier phases of thyroid development (“jag1b?”), due to its spotted pattern of expression in the region of the thyroid primordium origin at 24 hpf; jag1a is mainly expressed at 72 hpf, in the most anterior portion of the first thyroid follicle. By 72 hpf, the thyroid tissue starts to elongate posteriorly and produce T4. Jag1-Notch signaling sustains these steps and the maintenance of thyroid cells (dotted black arrow, 2). jag1 loss-of- function conditions impair thyroid development and function (black arrow, 3). T, Thyroid; ch, ceratohyal; h, heart. Stages, upper part of the panel; 24 and 36 hpf, transversal views; from 48 to 120 hpf, ventral views.
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FIG. 8. Model describing the role of Notch signaling and <t>Jag1-Notch</t> interaction in zebrafish thyroid development. The thyroid primordium originates from the pharyngeal endoderm by 24 hpf. Our data indicate that Notch signaling originating from the endodermal layer itself or from the surrounding developing tissues plays a fundamental role in limiting the number of thyroidal differentiating precursors (double dotted arrow, 1, left side of the panel). The combined expression of nkx2.1a, pax2a, hhex, and pax8 is distinctive of the thyroid follicular cells. jag1b is mainly expressed starting from at 48 hpf; nevertheless, we can not completely exclude jag1b contribution in earlier phases of thyroid development (“jag1b?”), due to its spotted pattern of expression in the region of the thyroid primordium origin at 24 hpf; jag1a is mainly expressed at 72 hpf, in the most anterior portion of the first thyroid follicle. By 72 hpf, the thyroid tissue starts to elongate posteriorly and produce T4. Jag1-Notch signaling sustains these steps and the maintenance of thyroid cells (dotted black arrow, 2). jag1 loss-of- function conditions impair thyroid development and function (black arrow, 3). T, Thyroid; ch, ceratohyal; h, heart. Stages, upper part of the panel; 24 and 36 hpf, transversal views; from 48 to 120 hpf, ventral views.
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Image Search Results


FIG. 8. Model describing the role of Notch signaling and Jag1-Notch interaction in zebrafish thyroid development. The thyroid primordium originates from the pharyngeal endoderm by 24 hpf. Our data indicate that Notch signaling originating from the endodermal layer itself or from the surrounding developing tissues plays a fundamental role in limiting the number of thyroidal differentiating precursors (double dotted arrow, 1, left side of the panel). The combined expression of nkx2.1a, pax2a, hhex, and pax8 is distinctive of the thyroid follicular cells. jag1b is mainly expressed starting from at 48 hpf; nevertheless, we can not completely exclude jag1b contribution in earlier phases of thyroid development (“jag1b?”), due to its spotted pattern of expression in the region of the thyroid primordium origin at 24 hpf; jag1a is mainly expressed at 72 hpf, in the most anterior portion of the first thyroid follicle. By 72 hpf, the thyroid tissue starts to elongate posteriorly and produce T4. Jag1-Notch signaling sustains these steps and the maintenance of thyroid cells (dotted black arrow, 2). jag1 loss-of- function conditions impair thyroid development and function (black arrow, 3). T, Thyroid; ch, ceratohyal; h, heart. Stages, upper part of the panel; 24 and 36 hpf, transversal views; from 48 to 120 hpf, ventral views.

Journal: Endocrinology

Article Title: Disruptions of global and JAGGED1-mediated notch signaling affect thyroid morphogenesis in the zebrafish.

doi: 10.1210/en.2011-1888

Figure Lengend Snippet: FIG. 8. Model describing the role of Notch signaling and Jag1-Notch interaction in zebrafish thyroid development. The thyroid primordium originates from the pharyngeal endoderm by 24 hpf. Our data indicate that Notch signaling originating from the endodermal layer itself or from the surrounding developing tissues plays a fundamental role in limiting the number of thyroidal differentiating precursors (double dotted arrow, 1, left side of the panel). The combined expression of nkx2.1a, pax2a, hhex, and pax8 is distinctive of the thyroid follicular cells. jag1b is mainly expressed starting from at 48 hpf; nevertheless, we can not completely exclude jag1b contribution in earlier phases of thyroid development (“jag1b?”), due to its spotted pattern of expression in the region of the thyroid primordium origin at 24 hpf; jag1a is mainly expressed at 72 hpf, in the most anterior portion of the first thyroid follicle. By 72 hpf, the thyroid tissue starts to elongate posteriorly and produce T4. Jag1-Notch signaling sustains these steps and the maintenance of thyroid cells (dotted black arrow, 2). jag1 loss-of- function conditions impair thyroid development and function (black arrow, 3). T, Thyroid; ch, ceratohyal; h, heart. Stages, upper part of the panel; 24 and 36 hpf, transversal views; from 48 to 120 hpf, ventral views.

Article Snippet: For Jag1 immunofluorescence on mouse thyroid tissue, sections (5 m) cut from OCT-embedded tissue blocks were blocked with 1% BSA/2% donkey serum and immunostained overnight at 4 C with Jagged1 polyclonal antibody (1:100, H-114; Santa Cruz Biotechnology, Inc., Santa Cruz, CA).

Techniques: Expressing