Accumulation of components of basal laminae: Association with the failure of neural crest cells to colonize the presumptive aganglionic bowel of mutant mice

Payette, Robert F.; Tennyson, Virginia M.; Pomeranz, Howard D.; Pham, Tuan D.; Rothman, Taube P.; Gershon, Michael D.

doi:10.1016/0012-1606(88)90217-5

Cited by 104 publications

(54 citation statements)

References 35 publications

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“…Prior in vitro studies (Haffen et al, 1981(Haffen et al, , 1983Kedinger et al, 1986Kedinger et al, , 1990Payette et al, 1988;Weiser et al , 1990) have clearly demonstrated that endodermal cells derived from the intestine can reciprocally induce associated mesenchymal cells to differentiate into smooth muscle. The results of this study indicate that direct cell-cell contact between the developing endoderm and mesenchyme is not required for the initiation of smooth muscle development in the gastrointestinal tract, and suggest a putative role for diffusible factors1 gradients in the primary induction of gastrointestinal smooth muscle development.…”

Section: E-l 4h-k) This Differentiating Ring Of Smooth Mus-mentioning

confidence: 99%

“…Even so, the differentiation of longitudinal smooth muscle myoblasts in the developing gut appears coincident with the association of enteric neurons with the circular smooth muscle layer. Studies in the lethal spotted mouse (Payette et al, 1988) showed that segmental aganglionosis resulted in dramatic morphological changes in the muscularis propria of the affected bowel segment. These included hypertrophy/reduction in the number of smooth muscle myoblasts in the circular smooth muscle layer, as well as incomplete differentiation and misorientation of smooth muscle myoblasts in the longitudinal smooth muscle layer.…”

Section: E-l 4h-k) This Differentiating Ring Of Smooth Mus-mentioning

confidence: 99%

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Molecular analysis of smooth muscle development in the mouse

McHugh

1995

Developmental Dynamics

131

117

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Little is currently known regarding the ontogeny of smooth muscle tissues during normal mammalian development. The a-smooth muscle and y-smooth muscle isoactins have been shown to be excellent molecular markers of smooth muscle cell phenotype. This study characterizes both the temporal and spatial patterns of a-smooth muscle and y-smooth muscle isoactin expression in the developing mouse. In situ analysis was performed on serial sections of whole mouse embryos on embryonic day 9,11,13, 15, and 17 using a-smooth muscle and y-smooth muscle isoactin-specific riboprobes. Distinct temporal and spatial patterns of a-smooth muscle and y-smooth muscle isoactin gene expression were observed in the developing gastrointestinal tract, urogenital tract, respiratory tract, and vascular system. Independent expression of the a-smooth muscle isoactin was observed during the early stages of skeletal, cardiac, and smooth muscle myogenesis as well as in a novel subset of distinct organs including the postanal component of the hindgut, allantois, and primitive placenta. The results of this study indicate that distinct cellular phenotypes are involved in smooth muscle myogenesis and suggest that organ-specific mechanisms might exist for the initiation of smooth muscle development in vivo. In addition, the pattern of independent a-smooth muscle isoactin expression observed in this study provides novel information regarding the early stages of hindgut and placental development, and suggests that a common functional phenotype may be associated with the early stages of skeletal, cardiac, and smooth muscle myogenesis. 0 1995 Wiley-Liss, Inc.

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Section: E-l 4h-k) This Differentiating Ring Of Smooth Mus-mentioning

confidence: 99%

Section: E-l 4h-k) This Differentiating Ring Of Smooth Mus-mentioning

confidence: 99%

Molecular analysis of smooth muscle development in the mouse

McHugh

1995

Developmental Dynamics

131

117

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“…The nervous system of the affected region in the Hoxa-4-transgenic animals might be normal, but the smooth muscle could be abnormal and unable to propel intestinal contents. Abnormalities of smooth muscle, as well as nerve, have been described in the aganglionic region of the bowel of lslls mice (Tennyson et al, 1986;Payette et al, 1988). Our observations suggest that megacolon does arise in Hoxa-4-transgenic mice because the ENS is locally abnormal in the terminal gut; however, in contrast t o lslls mice, the defect appears to involve the development of hypoganglionosis and an inappropriate pattern of innervation, rather than aganglionosis.…”

mentioning

confidence: 52%

“…This defect is also found in the young adult transgenic mouse. Our previous studies of fetal lslls mice showed that there was an overabundance of laminin, hyaluronic acid, and proteoglycans that (i) preceded the formation of enteric ganglia, (ii) was in the path through which enteric neural precursors from the neural crest would have t o migrate, and (iii) was limited to the aganglionic and hypoganglionic segments of the lslls bowel (Payette et al, 1988, Tennyson et al, 1990a. These data are consistent with the hypothesis that components of basal laminae contributed to the inability of crest-derived cells to colonize the terminal bowel of lslls mice.…”

Section: Similarities and Differences Between Transgenic And Islls Micementioning

confidence: 99%

“…In vitro development of immunoselected crest-derived cells as neurons and glia is promoted by laminin (Pomeranz et al, 1993). Conceivably an excess of the laminin in the presumptive aganglionic zone of the lslls gut (Tennyson et al, 1986(Tennyson et al, , 1990aPayette et al, 1988) causes migrating crest-derived cells to stop prematurely. If neurons differentiate too soon, the region distal to the zone where the abnormal environment is encountered will become aganglionic.…”

Section: Similarities and Differences Between Transgenic And Islls Micementioning

confidence: 99%

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Structural abnormalities associated with congenital megacolon in transgenic mice that overexpress the Hoxa‐4 gene

Tennyson

Gershon

Sherman

et al. 1993

Developmental Dynamics

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Congenital megacolon develops in transgenic mice that overexpress the homeobox-containing gene, Hoxu-4. The current study was done to identify abnormalities of the terminal colon that might account for the phenotype. The terminal bowel of transgenic mice was compared with that of control and lethal spotted (ZslZs) mice, a strain in which megacolon also develops. The terminal colon of the transgenic mice contained fewer ganglia than that of controls, but was hypoganglionic, rather than aganglionic like that of ZslZs mice. The neurons present in the adult transgenic colon were significantly increased in size and a subset of very large neurons (>40 p. m in maximum diameter) were observed. Electron microscopic studies of young adult transgenic mice revealed that the ganglia and nerves of the myenteric plexus had the ultrastructure of extraenteric peripheral nerve rather than that of the enteric nervous system (ENS). The myenteric ganglia in the transgenic animals contained Schwann cells associated with a basal lamina that enveloped axons completely and individually, instead of glia. Although collagen is excluded from the ganglia and thin nerve fibers of the normal ENS, a collagen-containing endoneurium surrounded each of the axon-Schwann cell units of the abnormal nerve fibers of the transgenic colon. Some of the neurons of the transgenic mice were located in these nerve bundles rather than in ganglia. There were also smooth muscle abnormalities in the terminal bowel of the transgenic mice. Wide gaps were present in the longitudinal muscle of the transgenic mice; these gaps contained ganglia that were in contact with the adventitia. These longitudinal smooth muscle cells were more irregular than those of controls and they contained fewer puncta adherens; moreover, a larger proportion of the volume of the cytoplasm of transgenic smooth muscle cells was occupied by organelles. Finally, an extensive thickening and reduplication of the basal lamina surrounding the smooth muscle cells of the muscularis mucosa was observed in the transgenic colon and resembled 0 1993 WILEY-LISS, INC.that found in ZslZs mice. These data suggest that both smooth muscle and the innervation of the terminal bowel of neonatal Hoxu-4 transgenic mice are structurally abnormal. Although some of the abnormalities seen in Hoxu-4 transgenic mice are similar to those which arise in Zslls mice, the two conditions are not identical. In both animals, the data are consistent with the hypothesis that the defects arise as a result of a defective interaction between the precursors of enteric neurons and smooth muscle. o 1993 Wiley-Liss, Inc.

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