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1. |
Expression of the platelet‐derived growth factor β receptor during organogenesis and tissue differentiation in the mouse embryo |
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Developmental Dynamics,
Volume 199,
Issue 3,
1994,
Page 169-175
E. Shinbrot,
K. G. Peters,
L. T. Williams,
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摘要:
AbstractIn this study we used in situ hybridization to localize expression of the platelet‐derived growth factor β (PDGFβ) receptor mRNA during organogenesis in the mouse embryo (E 9.5–16.5). Expression was first seen in periaortic mesenchyme (E 9.5–10.5). Later (E 12.5–E 16.5), the receptor was expressed in the mesenchymal component of many developing tissues and organs, particularly derivatives of the primitive gut. The expression was exceptionally high in mesenchyme directly supporting an epithelium, typical of many developing organs such as the trachea and intestine. However, as the mesenchyme differentiated into smooth muscle, PDGFβ receptor mRNA was no longer detected. The expression of the PDGFβ receptor mRNA in mesenchymal components of developing organs, along with its absence in epithelial tissues, indicates that it may play a role in mesenchymal‐epithelial interactions during organ development. Somewhat unexpectedly, the PDGFβ receptor was highly expressed in the endothelium of small blood vessels and vascular structures such as the hyaloid plexus and choroid plexus. In large blood vessels, PDGFβ receptor mRNA was found in the mesenchyme surrounding the endothelium. This suggests that the PDGFβ receptor is involved in growth and development of blood vessels. © 199
ISSN:1058-8388
DOI:10.1002/aja.1001990302
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1994
数据来源: WILEY
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2. |
Apoptosis in human skin development: Morphogenesis, periderm, and stem cells |
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Developmental Dynamics,
Volume 199,
Issue 3,
1994,
Page 176-188
Renata R. Polakowska,
Mauro Piacentini,
Russell Bartlett,
Lowell A. Goldsmith,
Anne R. Haake,
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摘要:
AbstractDuring human skin development, embryonic‐ and fetal‐specific periderm cells and incompletely keratinized cells are replaced by keratinocytes that differentiate while stratifying to form the fully functional epidermis. Proliferating basal cells of fetal skin also develop into epidermal appendages such as hair follicles and glands. We demonstrate that programmed cell death, not emphasized in conventional epidermal biology, has an important function in establishing the final architecture of the human epidermis and its appendages. Immunohistochemical localization of transglutaminases in fetal periderm, intermediate epidermal cells, and within appendages coincides with DNA fragmentation indicating that apoptosis is involved in deletion of these stage‐specific cells and remodeling of appendages. The data also suggest that terminal differentiation of epidermal cells might be a specialized form of apoptosis. The pattern of expression of bcl‐2, a gene associated with survival of some cells, is exclusive of the distribution patterns of markers of the cell death pathway. Bcl‐2 protein is correlated with specific morphogenetic events in hair follicles and eccrine sweat glands, and its presence in single cells of the hair follicle bulge suggests that Bcl‐2 may be a stem cell marker. © 1994 Wil
ISSN:1058-8388
DOI:10.1002/aja.1001990303
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1994
数据来源: WILEY
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3. |
Regulation ofamelogeningene expression during tooth development |
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Developmental Dynamics,
Volume 199,
Issue 3,
1994,
Page 189-198
Enhong Chen,
Ronald Piddington,
Sylvia Decker,
Jonathan Park,
Zhi‐An Yuan,
William R. Abrams,
Joel Rosenbloom,
George Feldman,
Carolyn W. Gibson,
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摘要:
AbstractThe amelogenins are the predominant matrix proteins in developing enamel and are crucial for proper enamel mineralization. Transgenic mice were constructed in order to identify the segment of theamelogeningene required for specific expression in enamel organ cells. A 3.5 kb fragment of the bovine X‐chromosomalamelogeningene that includes a TATA box, the transcription initiation site, and 32 bp of exon 1 was linked to the βgalactosidasegene and injected into fertilized mouse eggs. Newborn transgene positive mice expressed βgalactosidase activity in developing teeth treated with the chromogenic substrate Xgal. Foci of ameloblasts were positive in newborn mice; stain intensity and number of positive ameloblasts increased in 1‐day and 2‐day postnatal mice. Some of the adjacent stratum intermedium cells also were positive in the later stages. Targeting of the transgene to the enamel organ was specific; the only other cells observed to be positive were macrophages, which have endogenous βgalactosidase activity. © 1994 Wiley
ISSN:1058-8388
DOI:10.1002/aja.1001990304
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1994
数据来源: WILEY
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4. |
Stage and tissue‐specific expression of the alcohol dehydrogenase 1 (Adh‐1) gene during mouse development |
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Developmental Dynamics,
Volume 199,
Issue 3,
1994,
Page 199-213
Jean‐Luc Vonesch,
Harikrishna Nakshatri,
Murielle Philippe,
Pierre Chambon,
Pascal Dollé,
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摘要:
AbstractTheAdh‐1gene product, ADH‐A2, the only known murine class I alcohol dehydrogenase, is able to oxidize retinol (vitamin A) into retinaldehyde, the first enzymatic step in the conversion of retinol into its biologically active metabolite retinoic acid. We have investigated the developmental expression pattern ofAdh‐1transcripts by in situ hybridization. Transcripts were first detected by embryonic day 10.5 in the mesonephros mesenchyme. During the following gestational days,Adh‐1transcripts were detected in several mesenchymal areas, such as nasal, laterocervical, and genital regions.Adh‐1transcripts were also detected in a small ectodermal domain at the anterior margins of both forelimbs and hindlimbs. During late fetal development,Adh‐1transcripts were found essentially in the epidermis and in a number of tissues which continue to express the gene after birth, such as liver, kidney, gut epithelium, adrenal cortex, testis interstitium, and ovarian stroma. In contrast, a strong expression ofAdh‐1was found in the mesenchyme of developing lungs, but not in the adult organ. This highly regulated expression ofAdh‐1is discussed with respect to the local synthesis of retinoic acid during development. Although the promoter of the human counterpart ofAdh‐1contains a retinoic acid response element (Duester et al. [1991] Mol. Cell. Biol. 11:1638–1646), we report that this element is not conserved in the murine gene. Consistently,Adh‐1promoter‐containing reporter constructs were not retinoic acid‐inducible in cotransfections assays with RARs and/or RXRs, suggesting that retinoic acid regulation ofAdh‐1differs from that of the human g
ISSN:1058-8388
DOI:10.1002/aja.1001990305
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1994
数据来源: WILEY
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5. |
Deficient outgrowth of the ureteric bud underlies the renal agenesis phenotype in mice manifesting thelimb deformity (ld) mutation |
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Developmental Dynamics,
Volume 199,
Issue 3,
1994,
Page 214-228
Richard Maas,
Sandra Elfering,
Tom Glaser,
Lisa Jepeal,
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摘要:
AbstractMice which are homozygous for thelimb deformity (ld)mutation also manifest an incompletely penetrant unilateral or bilateral renal agenesis phenotype. Intercross experiments suggest that the differences in penetrance of the renal agenesis phenotype between homozygous mice with differentldalleles are due to intrinsic differences in the strength of the mutant alleles or to one or more closely linked modifying loci, and not to generalized differences in genetic background. Analysis ofld/ldembryos between embryonic days 11–13 reveals delayed outgrowth or complete absence of the ureteric bud, the inducer of metanephric mesenchyme. Since explants ofld/ldmetanephric mesenchyme differentiate in culture when apposed to embryonic spinal cord, we conclude that deficient ureteric bud outgrowth is the morphologic basis for renal agenesis inld/ldmice. However, sinceldtranscripts can be detected in both metanephric mesenchyme and ureteric bud, the molecular basis for the deficiency in ureteric bud outgrowth could reside in either component. © 1994 Wiley‐Liss,
ISSN:1058-8388
DOI:10.1002/aja.1001990306
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1994
数据来源: WILEY
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6. |
Forward spreading in the establishment of a vertebrate Hox expression boundary: The expression domain separates into anterior and posterior zones, and the spread occurs across implanted glass barriers |
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Developmental Dynamics,
Volume 199,
Issue 3,
1994,
Page 229-240
Stephen J. Gaunt,
Lorna Strachan,
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摘要:
AbstractBy use of wholemount in situ hybridization, we show how expression of the chicken homeobox geneHoxd‐4commences in the posterior part of the primitive streak and then spreads forward, covering most of the primitive streak by the 2 somite stage, covering the entire primitive streak by the 5 somite stage, reaching the somite 1/somite 2 level of the neural tube by the 9 somite stage, and reaching the rhombomere 6/rhombomere 7 junction of the hindbrain by the 15 somite stage. Forward spreading does not depend upon cell migration, as was evidenced by vital dye (DiI) cell marking experiments. Furthermore, forward spreading does not apparently require tissue continuity since it could not be blocked by impermeable (glass) barriers surgically implanted to divide embryonic tissues. As forward spreading of chickHoxd‐4proceeds, the domain of expression separates, at late primitive streak stages, into “anterior” and “posterior zones,” with an intervening “intermediate zone” of weak or non‐expression. Clear anterior and posterior zones were also found forHoxa‐3anda‐4expression in late primitive steak stage mouse embryos. We present evidence that the anterior zone corresponds with the “definitive” domain of Hox gene expression, as has earlier been extensively characterized in midgestation embryos. The posterior zone is transitory, probably persisting only for the duration of the primitive streak, and it is a region of intense Hox expression in primitive streak tissue, Hensen's node, and adjacent regions of neurectoderm and mesoderm. We suggest that the posterior zone marks the source of a morphogen which is the primary activator of Hox gene expression, and we discuss possible models for the mechanism of forward spreading in expressio
ISSN:1058-8388
DOI:10.1002/aja.1001990307
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1994
数据来源: WILEY
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7. |
Developmental expression of human cartilage matrix protein |
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Developmental Dynamics,
Volume 199,
Issue 3,
1994,
Page 241-252
S. Mundlos,
B. Zabel,
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摘要:
AbstractCartilage matrix protein (CMP) is a non‐collagenous component of cartilage with a yet unknown function. In this study we used in situ hybridization to investigate the temporal and sptial distribution of CMP transcripts during human embryonic and early fetal development, and compared it to the pattern of expression observed for collagen types I, II, X, and decorin. The distribution of CMP and collagen type II transcripts followed a similar pattern in the embryonic bone anlage, the fetal growth plate, and the developing vertebral column. Expression was highest in the upper hypertrophic and lower proliferative zone, whereas calcified cartilage was negative throughout the different stages of bone development. Chondrocytes of calcified cartilage, however, were not quiescent but expressed collagen type X. The onset of collagen type X expression was linked to hypertrophy and occurred before calcification became apparent. In contrast, deorin and collagen type I were highly expressed in bone and perichondrium but not in growth plate cartilage. During the development of the synovial joints a different pattern of expression emerged. After formation of the joint cavity, there was a halt in expression of CMP but not of collagen type II in chondrocytes close to the articular surface. A band of CMP negative chondrocytes covering the joint surface was observed in all joints investigated. Decorin mRNA was demonstrated in the reserve zone adjacent to the joints, but not in articular cartilage. Extraskeletal expression of CMP was observed in the embryonic retina. The results demonstrate the differential expression of CMP during human skeletal development and chondrocyte differentiation. The distribution of CMP transcripts is unique and distinct from other known matrix genes. © 1994 Wiley‐Liss,
ISSN:1058-8388
DOI:10.1002/aja.1001990308
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1994
数据来源: WILEY
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8. |
Masthead |
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Developmental Dynamics,
Volume 199,
Issue 3,
1994,
Page -
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PDF (42KB)
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ISSN:1058-8388
DOI:10.1002/aja.1001990301
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1994
数据来源: WILEY
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