The location of the pregut endoderm in the chick embryo at the primitive streak stage as determined by radioautographic mapping

Rosenquist, Glenn C.

doi:10.1016/0012-1606(71)90131-x

Cited by 96 publications

(57 citation statements)

References 15 publications

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“…Our in vivo implantation study demonstrated that the mesoderm on the left side has the competence to respond to an ectopic liver budderived inductive influence, favoring the former possibility. However, before Wt1 and capsulin expression becomes detectable, progenitors of the liver bud are located bilaterally (Matsushita, 1996;Rosenquist, 1971), similar to those in mouse embryos (Tremblay and Zaret, 2005), in which PE develops bilaterally. Therefore, it is possible that non-liver tissues negatively regulate PE development specifically on the left side of the pericardial mesoderm, although nothing is known about an activity that antagonizes PE development.…”

Section: Inductive Interaction(s) Between the Liver Bud And Mesotheliumsupporting

confidence: 60%

Induction of proepicardial marker gene expression by the liver bud

et al. 2007

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Cells of the coronary vessels arise from a unique extracardiac mesothelial cell population, the proepicardium, which develops posterior to the sinoatrial region of the looping-stage heart. Although contribution of the proepicardial cells to cardiac development has been studied extensively, it remains unresolved how the proepicardium is induced and specified in the mesoderm during embryogenesis. It is known, however, that the proepicardium develops from the mesothelium that overlays the liver bud. Here, we show that the expression of proepicardial marker genes -Wt1, capsulin (epicardin, pod1, Tcf21) and Tbx18, can be induced in naïve mesothelial cells by the liver bud, both in vitro and in vivo. Lateral embryonic explants, when co-cultured with the liver bud, were induced to express these proepicardial marker genes. The same induction of the marker genes was detected in vivo when a quail liver bud was implanted in the posterior-lateral regions of a chick embryo. This ectopic induction of marker gene expression was not evident when other endodermal tissues, such as the lung bud or stomach, were implanted. This inductive response to the liver bud was not detectable in host embryos before stage 12 (16-somite stage). These results suggest that, after a specific developmental stage, a large area of the mesothelium becomes competent to express proepicardial marker genes in response to localized liver-derived signal(s). The developmentally regulated competency of mesothelium and a localized inductive signal might play a role in restricting the induction of the proepicardial marker gene expression to a specific region of the mesothelium. The data might also provide a foundation for future engineering of a coronary vascular progenitor population.

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Section: Inductive Interaction(s) Between the Liver Bud And Mesotheliumsupporting

confidence: 60%

Induction of proepicardial marker gene expression by the liver bud

et al. 2007

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“…With tritiated thymidine, all cells of transplanted tissues may not be labeled (cells must be in the S phase of the cycle during exposure to become labeled), the label is diluted with each cell division, and the possibility exists that label can pass from grafts to neighboring host tissues during subsequent development. Although in some studies these problems are believed not to have been serious (see especially Rosenquist, 1966Rosenquist, , 1971a it is unclear to what extent they confound the results. Furthermore, the mesoderm maps in previous studies frequently included results obtained from grafts placed either completely lateral to the primitive streak or on the primitive streak and flanking areas (see Rosenquist, 1966: Fig. 1; Nicolet, 1970: Fig.…”

Section: Introductionmentioning

confidence: 99%

Mesoderm movement and fate during avian gastrulation and neurulation

Schoenwolf

García‐Martínez

Dias

1992

Developmental Dynamics

215

143

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Quail/chick transplantation chimeras were constructed during stages of gastrulation and neurulation to follow the subsequent movement and fate of cells of the primitive streak. All grafts were placed solely within the confines of the primitive streak to prevent confusion between cells that had not yet ingressed and those that had already ingressed, and transplanted cells were distinguished from host cells on the basis of a naturally occurring cell marker. Pathways of movement of ingressing cells corresponded to their level of residence within the primitive streak. Cells residing within Hensen's node (the cranial end of the primitive streak) initially migrated mainly cranially, remaining on or near the midline, and then extended caudally along the midline as regression of Hensen's node occurred. Cells residing within the nodus posterior (the caudal end of the primitive streak) migrated caudally. Cells residing at levels of the primitive streak between Hensen's node and the nodus posterior typically migrated bilaterally, confirming that such cells had not already ingressed prior to their transplantation (in which case, they would have migrated unilaterally). Subsets of these cells residing at progressively more caudal levels of the primitive streak migrated incrementally more laterally. Hensen's node contributed cells to the gut endoderm, head mesenchyme, notochord, and median hinge‐point (MHP) cells of the neural tube (future floor plate). At younger stages (i.e., stages 3a, 3b) Hensen's node contributed cells to principally the foregut endoderm and head mesenchyme, where‐as at older stages (i.e., stages 3c, 3d, 4), it contributed cells to principally the notochord and MHP region. The remaining segments of the cranial half of the primitive streak contributed cells to the various mesodermal subdivisions of the embryo, and the lengths of the segments forming these subdivisions were estimated. The most cranial level of the streak (directly behind Hensen's node) contributed cells to the most medial mesodermal subdivisions (head mesenchyme, somites) and consecutively more caudal levels of the streak contributed cells to sequentially more lateral mesodermal subdivisions (intermediate mesoderm, lateral plate mesoderm). The caudal half of the primitive streak contributed cells to the extraembryonic mesoderm, with the nodus posterior contributing cells to the most caudal extraembryonic mesoderm, including the blood islands. Our results confirm and extend the previous avian prospective fate maps, increasing our understanding of the movement and fate of cells of the gastrula and neurula stages. © 1992 Wiley‐Liss, Inc.

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“…During gastrulation, the chick embryo needs to reorganize its extraembryonic endodermal tissues (called hypoblast and endoblast) around newly generated DE. A series of fate-mapping experiments initially suggested an equivalent to the murine displacement model, namely that DE precursors ingressed at the primitive streak and inserted into the extraembryonic endoderm tissues, gradually displacing them to the periphery of the embryo where they would contribute primarily to extraembryonic tissues [76][77][78][79][80]. These fate-mapping experiments were performed with techniques such as carbon particle and vital dye staining that proved sufficient to look at mass movements, but did not provide sufficient resolution to address the movements of all cells and their individual dynamics.…”

Section: A Universal Cell Dispersal Mechanism Driving Endoderm Morphomentioning

confidence: 99%

Gutsy moves in mice: cellular and molecular dynamics of endoderm morphogenesis

Viotti¹,

Foley

Hadjantonakis

2014

Phil. Trans. R. Soc. B

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Despite the importance of the gut and its accessory organs, our understanding of early endoderm development is still incomplete. Traditionally, endoderm has been difficult to study because of its small size and relative fragility. However, recent advances in live cell imaging technologies have dramatically expanded our understanding of this tissue, adding a new appreciation for the complex molecular and morphogenetic processes that mediate gut formation. Several spatially and molecularly distinct subpopulations have been shown to exist within the endoderm before the onset of gastrulation. Here, we review findings that have uncovered complex cell movements within the endodermal layer, before and during gastrulation, leading to the conclusion that cells from primitive endoderm contribute descendants directly to gut.

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The location of the pregut endoderm in the chick embryo at the primitive streak stage as determined by radioautographic mapping

Cited by 96 publications

References 15 publications

Induction of proepicardial marker gene expression by the liver bud

Induction of proepicardial marker gene expression by the liver bud

Mesoderm movement and fate during avian gastrulation and neurulation

Gutsy moves in mice: cellular and molecular dynamics of endoderm morphogenesis

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