bluuebunny/crossref_metadata_2025_split huggingface dataset:
Selective regeneration of photoreceptors in goldfish retina
Authors: Braisted Janet E. , Essman Thomas F. , Raymond Pamela A. 
Published: April 2021

ABSTRACT
Previous work has shown that the neural retina in adult goldfish can regenerate. Following retinal damage elicited by surgical or cytotoxic lesions, missing neurons are replaced by foci of proliferating neuroepithelial cells, which previous studies have suggested are derived from rod pre-cursors. In the intact retina, rod precursors proliferate but produce only new rods. The regenerative responses observed previously have involved replacement of neurons in all retinal layers; selective regeneration of specific neuronal types (except for rod photoreceptors) has not been reported. In the experiments described here, we specifically destroyed either cones alone or cones and rods with an argon laser, and we found that both types of photoreceptors regenerated within a few weeks. The amount of cone regeneration varied in proportion to the degree of rod loss. This is the first demonstration of selective regenera-tion of a specific class of neuron (i.e., cones) in a region of central nervous tissue where developmental production of that class of neuron has ceased. Selective regeneration may be limited to photoreceptors, however, because when dopaminergic neurons in the inner retina were ablated with intraocular injections of 6-hydroxydopamine, in combination with laser lesions that destroyed photoreceptors, the dopaminergic neurons did not regenerate, but the photoreceptors did. These data support previous studies which showed that substantial cell loss is required to trigger regeneration of inner retinal neurons, including dopaminergic neurons. New observations here bring into question the presumption that rod precursors are the only source of neuronal progenitors during the regenerative response. Finally, a model is presented which suggests a possible mechanism for regulating the phenotypic fate of retinal progenitor cells during retinal regeneration.
An activated Notch suppresses neurogenesis and myogenesis but not gliogenesis in mammalian cells
Authors: Nye Jeffrey S. , Kopan Raphael , Axel Richard 
Published: April 2021

ABSTRACT
P19 cells, a mouse embryonal carcinoma line, can be induced to differentiate into neurons. After induction, however, only a small subpopulation of cells develop as neurons, suggesting that equipotent cells adopt different cell fates. In invertebrate systems, the lin-12-Notch family of genes is thought to control the choice of cell fate. We have therefore asked whether activation of murine Notch (mNotch) regulates neuronal differentiation in P19 cells. We demonstrate that a dominant gain-of-function mutant of mNotch suppresses neurogenesis, as well as myogenesis in P19 cells. Overexpression of the full-length mNotch protein also suppresses neurogenesis. In contrast, the differentiation of glia is not affected by an activated mNotch homologue. These data indicate that mNotch may play a central role in the choice of cell fate in differentiating cells in culture and suggests that mNotch may play a similar role in the choice of fate in the developing mammalian embryo.
Embryonic origin of the Arabidopsis primary root and root meristem initials
Authors: Scheres Ben , Wolkenfelt Harald , Willemsen Viola , Terlouw Maarten , Lawson Emily , Dean Caroline , Weisbeek Peter 
Published: April 2021

ABSTRACT
The embryonic origin of the Arabidopsis root and hypocotyl region has been investigated using histological techniques and clonal analysis. Our data reveal the pattern of cell division in the embryo giving rise to the various initials within the root promeristem. A small region of the root at its connection with the hypocotyl appears not to be derived from the promeristem initials. This region contains two cortical cell layer and [3H]thymidine incorporation data suggest that it lacks postembryonic cell divisions. Sectors marked by transposon excision from the β-glucuronidase marker gene are used to investigate cell lineages giving rise to root and hypocotyl. The position of end points from sectors with embryonic origin show little variation and hence reveal preferred positions in the seedling for cells derived from different regions of the embryo. The radial extent of complete root sectors is consistent with the radial arrangement of root meristem initials at the heart stage of embryogenesis inferred from histological analysis. Using the clonal data, a fate map is constructed depicting the destiny of heart stage embryonic cell tiers, in the seedling root and hypocotyl. The variability in the sector end points indicates that distinct cell lineages are not restricted for root or hypocotyl fate. In contrast, derivatives of the hypophyseal cell do appear to be restricted to the columella and central cell region of the root.
Negative control of Xenopus GATA-2 by activin and noggin with eventual expression in precursors of the ventral blood islands
Authors: Walmsley Maggie E. , Guille Matthew J. , Bertwistle David , Smith James C. , Pizzey John A. , Patient Roger K. 
Published: April 2021

ABSTRACT
To increase our understanding of haematopoiesis during early vertebrate development, we have studied the expression pattern of the transcription factor GATA-2 in Xenopus embryos, and asked how this is regulated. We show that the blood island precursors of the ventral mesoderm express GATA-2 RNA at neural tube stages, some 5 hours before globin RNA is detected in their derivatives. Prior to this however, GATA-2 is expressed much more widely within the embryo. Maternal transcripts are uniformly distributed, and zygotic transcription is activated during gastrulation throughout ventral and lateral regions of the embryo, with expression highest in the sensorial ectoderm and only weak in the ventral mesoderm. The domain of GATA-2 expression in neurulae outlines the region of the neural plate and suggests a possible wider role in dorsoventral patterning.
To identify the signals involved in regulating this pattern of expression, we performed experiments with embryo explants. GATA-2 is activated autonomously in isolated animal caps and this activation is suppressed by the mesoderm-inducing factor activin, but not by FGF. Thus, the down-regulation of GATA-2 observed in the region of the Spemann organiser may be a response to an activin-like signal emanating from the dorsal-vegetal region or Nieuwkoop centre. GATA-2 activation in animal caps and ventral marginal zones was suppressed by co-culturing with dorsal marginal zones, suggesting that a signal from the Spemann organiser is involved in suppression of GATA-2 in the dorsal region of the embryo. Expression of a candidate for this signal, noggin, had the same effect. Taken together, the observations presented here suggest that GATA-2 activation occurs by default in the absence of signals, that the restriction of its expression within the early embryo is controlled by negative signals emanating from the Nieuwkoop centre and the organiser, and that noggin and activin-like molecules play a role in these signalling pathways.
Genetic control of sex determination in the germ line and soma of the housefly, Musca domestica
Authors: Hilfiker-Kleiner Denise , Dübendorfer Andreas , Hilfiker Andres , Nöthiger Rolf 
Published: April 2021

ABSTRACT
In Musca domestica, sex in the soma is cell autonomously determined by the male-determiner M, or by the female-determiner FD. Transplanted pole cells (precursors of the germ line) show that sex determination of germ cells is non-autonomous: genotypically male pole cells form functional eggs in female hosts, and genotypically female pole cells form functional sperm in male hosts. When M/+ cells undergo oogenesis, a male-determining maternal effect predetermines offspring without M, i.e. of female genotype, to develop as fertile males. FD is epistatic to M in the female germ line, as it is in the soma, overruling the masculinizing effect of M. The results suggest that maternal F product is needed for activation of the zygotic F gene.
Platelet endothelial cell adhesion molecule-1 (PECAM-1 / CD31): alternatively spliced, functionally distinct isoforms expressed during mammalian cardiovascular development
Authors: Baldwin H. Scott , Shen Hong Min , Yan Horng-Chin , DeLisser Horace M. , Chung Audrey , Mickanin Craig , Trask Timothy , Kirschbaum Nancy E. , Newman Peter J. , Albelda Steven M. , Buck Clayton A. 
Published: April 2021

ABSTRACT
The establishment of the cardiovascular system represents an early, critical event essential for normal embryonic development. An important component of vascular ontogeny is the differentiation and development of the endothelial and endocardial cell populations. This involves, at least in part, the expression and function of specific cell surface receptors required to mediate cell-cell and cell-matrix adhesion. Platelet endothelial cell adhesion molecule-1 (PECAM-1, CD31) may well serve such a function. It is a member of the immunoglobulin superfamily expressed by the entire vascular endothelium in the adult. It is capable of mediating adhesion by a heterophilic mechanism requiring glycosaminoglycans, as well as by a homophilic, glycosaminoglycan independent, mechanism. It has been shown to regulate the expression of other adhesion molecules on naive T cells. This report documents by RT-PCR and immunohistochemical analysis the expression of PECAM-1 during early post implantation mouse embryo development. PECAM-1 was expressed by early endothelial precursors first within the yolk sac and subsequently within the embryo itself. Interestingly, embryonic PECAM-1 was expressed as multiple isoforms in which one or more clusters of polypeptides were missing from the cytoplasmic domain. The sequence and location of the deleted polypeptides corresponded to exons found in the human PECAM-1 gene. The alternatively spliced isoforms were capable of mediating cell-cell adhesion when transfected into L-cells. The isoforms differed, however, in their sensitivity to a panel of anti-PECAM-1 monoclonal antibodies. These data suggest that changes in the cyto-plasmic domain of PECAM-1 may affect its function during cardiovascular development, and are consistent with our earlier report that systematic truncation of the cytoplasmic domain of human PECAM-1 resulted in changes in its ligand specificity, divalent cation and gly-cosaminoglycan dependence, as well as its susceptibility to adhesion blocking monoclonal antibodies. This is the first report of naturally occurring alternatively spliced forms of PECAM-1 having possible functional implications.
The helix-loop-helix extramacrochaetae protein is required for proper specification of many cell types in the Drosophila embryo
Authors: Cubas Pilar , Modolell Juan , Gómez Mar 
Published: April 2021

ABSTRACT
The Drosophila Extramacrochaetae protein antagonizes the proneural function of the Achaete and Scute proteins in the generation of the adult fly sensory organs. Extra-macrochaetae sequesters these basic-region-helix-loop-helix transcription factors as heterodimers inefficient for binding to DNA. We show that, during embryonic devel-opment, the extramacrochaetae gene is expressed in complex patterns that comprise derivatives of the three embryonic layers. Expression of extramacrochaetae often precedes and accompanies morphogenetic movements. It also occurs at regions of specialized cell-cell contact and/or cell recognition, like the epidermal part of the muscle attachment sites and the differentiating CNS. The insuffi-ciency of extramacrochaetae affects most tissues where it is expressed. The defects suggest faulty specification of different cell types and result in impairment of processes as diverse as cell proliferation and commitment, cell adhesion and cell recognition. If Extramacrochaetae par-ticipates in cell specification by dimerizing with basic-region-helix-loop-helix proteins, the variety of defects and tissues affected by the insufficiency of extramacrochaetae suggests that helix-loop-helix proteins are involved in many embryonic developmental processes.
Programmed cell death is affected in the novel mouse mutant Fused toes (Ft)
Authors: Hoeven Frank van der , Schimmang Thomas , Volkmann Ariane , Mattei Marie-Genevieve , Kyewski Bruno , Rüther Ulrich 
Published: April 2021

ABSTRACT
We have identified a novel dominant mouse mutant that is characterised by fused toes on the fore limbs and a thymic hyperplasia, in heterozygous animals. Homozygosity of the mutation leads to malformation of the developing brain, lost of the genetic control of left-right asymmetry and to death around day 10 of development. Analysis of both limb development and induction of apoptosis in immature thymocytes in vitro suggest that programmed cell death is affected by the mutation. Since the mutation was causedvia a transgene insertion we were able to map it to the D region on mouse chromosome 8. So far, no mutation that affects programmed cell death has been mapped to this chromosome. Thus, this mutation will allow the identification of a novel gene involved in programmed cell death during mammalian development.
The role of segment polarity genes during early oogenesis in Drosophila
Authors: Forbes Alexandria J. , Spradling Allan C. , Ingham Philip W. , Lin Haifan 
Published: April 2021

ABSTRACT
In the Drosophila ovary, hedgehog (hh) signaling from cells near the apical tip of the germarium stimulates the proliferation and specification of somatic cells in region 2 of the germarium, 2-5 cells away from the hh-expressing cells (A.J. Forbes, H. Lin, P. Ingham and A. Spradling (1996) Development 122, 1125-1135). This report examines the role during early oogenesis of several genes that are known to function in hh-mediated signaling during embryonic and larval development (P. Ingham (1995)Current Opin. Genetics Dev. 5, 528-534). As in imaginal discs, engrailed (en) is co-expressed with hh in the germarium, while patched (ptc) and cubitus interruptus (ci) are expressed in somatic cells throughout the germarium and in developing egg chambers, with ptc expression being elevated within 10 cell diameters of the source of the hh signal. Moreover, the somatic cell overproliferation caused by ectopic hh expression is accompanied by elevated levels of ptc and is phenocopied in ptc− somatic clones. These analyses suggest that ptc and ci are components of the hh signaling pathway in the germarium. However, unlike embryos and imaginal discs, neither wingless (wg) nor decapentaplegic (dpp) appear to mediate the ovarian hh signal. wg is expressed in ‘cap cells,’ a subset of hh-expressing cells located adjacent to germ-line stem cells, but is unaffected by ectopic hh expression. Nor does the ectopic expression of wg or dpp mimic the effect of ectopic hh expression. We propose that Hh diffuses from apical cells, including cap cells, and regulates the proliferation of nearby ovarian somatic cells by antagonizing the negative effects of ptc on ci activity in these cells, thereby allowing the transcription of ci-dependent genes, including ptc itself.
Immortalization of pituitary cells at discrete stages of development by directed oncogenesis in transgenic mice
Authors: Alarid Elaine T. , Windle Jolene J. , Whyte David B. , Mellon Pamela L. 
Published: April 2021

ABSTRACT
Targeted expression of oncogenes in transgenic mice can immortalize specific cell types to serve as valuable cultured model systems. Utilizing promoter regions from a set of genes expressed at specific stages of differentiation in a given cell lineage, we demonstrate that targeted oncogenesis can produce cell lines representing sequential stages of development, in essence allowing both spatial and temporal immortalization. Our strategy was based on our production of a committed but immature pituitary gonadotrope cell line by directing expression of the oncogene SV40 T antigen using a gonadotrope-specific region of the human glycoprotein hormone α-subunit gene in transgenic mice. These cells synthesize α-subunit and gonadotropinreleasing hormone (GnRH) receptor, yet are not fully differentiated in that they do not synthesize the β-subunits of luteinizing hormone (LH) or follicle-stimulating hormone (FSH). This observation lead to the hypothesis that targeting oncogenesis with promoters that are activated earlier or later in development might immortalize cells that were more primitive or more differentiated, respectively. To test this hypothesis, we used an LHβ promoter to immortalize a cell that represents a subsequent stage of gonadotrope differentiation (expression of α-subunit, GnRH receptor, and LH β-subunit but not FSH β-subunit). Conversely, targeting oncogenesis with a longer fragment of the human α-subunit gene (which is activated earlier in development) resulted in the immortalization of a progenitor cell that is more primitive, expressing only the α-subunit gene. Interestingly, this transgene also immortalized cells of the thyrotrope lineage that express both α- and β-subunits of thyroid-stimulating hormone and the transcription factor GHF-1 (Pit-1). Thus, targeted tumorigenesis immortalizes mammalian cells at specific stages of differentiation and allows the production of a series of cultured cell lines representing sequential stages of differentiation in a given cell lineage.
The dominant white spotting oncogene allele KitW-42J exacerbates XYDOM sex reversal
Authors: Nagamine Claude M. , Carlisle Cherlynn 
Published: April 2021

ABSTRACT
The Y chromosome from certain populations of M. m. domesticus is incapable of normal testis determination in the B6 inbred strain resulting in XY hermaphrodites or XY females (XYDOM sex reversal). B6 consomic strains have been developed with either transient (B6-YAKR) or severe (B6-YTIR) XYDOM sex reversal. We report that a point mutation, the dominant white spotting oncogene allele, KitW-42J, exacerbates XYDOM sex reversal. In B6-YAKR, penetrance of the trait is low; however, in B6-YTIR, KitW-42J exacerbated sex reversal to such an extent that almost all XY progeny developed into females. The exacerbation of sex reversal was not linked to retardation of early fetal growth or reduction of testis size. Furthermore, semiquantitative RT-PCR for the testis-determining gene, Sry, suggests that exacerbation of sex reversal in B6-YTIR is not due to blockade of Sry expression, a substantial delay in initiation of Sry expression, or exceptionally low levels of Sry mRNAs. We propose that KitW-42J enhances sex reversal by adversely affecting a critical step in testis differentiation that is downstream of Sry.
BMP-2/-4 mediate programmed cell death in chicken limb buds
Authors: Yokouchi Yuji , Sakiyama Jyun-ichi , Kameda Takashi , Iba Hideo , Suzuki Atsushi , Ueno Naoto , Kuroiwa Atsushi 
Published: April 2021

ABSTRACT
During limb development, the mesenchymal cells in restricted areas of limb bud, anterior necrotic zone, posterior necrotic zone, opaque zone and interdigital necrotic zones, are eliminated by programmed cell death. The transcripts of bone morphogenetic protein (Bmp)-2 and -4 were first detected in the areas where cell death was observed, then showed overlapping expression with the programmed cell death zones except the opaque zone. To investigate the function of BMP-2 and BMP-4 during limb pattern formation, the dominant negative form of BMP receptor was overexpressed in chick leg bud via a replication-competent retrovirus to block the endogenous BMP-2/-4 signaling pathway. This resulted in excess web formation at the anterior and posterior regions of limb buds in addition to marked suppression of the regression of webbing at the interdigital regions. Significant reductions in the number of apoptotic cells in these three necrotic zones were found in the limb buds which received the virus carrying dominant negative BMP receptor. This indicates that extra tissue formation is due to suppression of programmed cell death in the three necrotic zones. Moreover, BMP-2/-4 protein induced apoptosis of mesenchymal cells isolated from the interdigital region in vitro. Other TGFβ family proteins as TGFβ1 and Activin did not show this effect. These results suggest that BMP-2 and BMP-4 are the apoptotic signal molecules of the programmed cell death process in the chick limb buds.
Mutations that perturb poly(A)-dependent maternal mRNA activation block the initiation of development
Authors: Lieberfarb Marshal E. , Chu Tehyen , Wreden Christopher , Theurkauf William , Gergen J. Peter , Strickland Sidney 
Published: April 2021

ABSTRACT
Translational recruitment of maternal mRNAs is an essential process in early metazoan development. To identify genes required for this regulatory pathway, we have examined a collection of Drosophila female-sterile mutants for defects in translation of maternal mRNAs. This strategy has revealed that maternal-effect mutations in the cortex and grauzone genes impair translational activation and cytoplasmic polyadenylation of bicoid and Toll mRNAs. Cortex embryos contain a bicoid mRNA indistinguishable in amount, localization, and structure from that in wild-type embryos. However, the bicoid mRNA in cortex embryos contains a shorter than normal polyadenosine (poly(A)) tail. Injection of polyadenylated bicoid mRNA into cortex embryos allows translation, demonstrating that insufficient polyadenylation prevents endogenous bicoid mRNA translation. In contrast, nanos mRNA, which is activated by a poly(A)-independent mechanism, is translated in cortex embryos, indicating that the block in maternal mRNA activation is specific to a class of mRNAs. Cortex embryos are fertilized, but arrest at the onset of embryogenesis. Characterization of grauzone mutations indicates that the phenotype of these embryos is similar to cortex. These results identify a fundamental pathway that serves a vital role in the initiation of development.
Regulative capacity of the archenteron during gastrulation in the sea urchin
Authors: McClay David R. , Logan Catriona Y. 
Published: April 2021

ABSTRACT
Gastrulation in the sea urchin involves an extensive rearrangement of cells of the archenteron giving rise to secondary mesenchyme at the archenteron tip followed by the foregut, midgut and hindgut. To examine the regulative capacity of this structure, pieces of the archenteron were removed or transplanted at different stages of gastrulation. After removal of any or all parts of the archenteron, the remaining veg 1 and/or veg 2 tissue regulated to replace the missing parts. Endoderm transplanted to ectopic positions also regulated to that new position in the archenteron. This ability to replace or regulate endoderm did not decline until after full elongation of the archenteron was completed. When replacement occurred, the new gut was smaller relative to the remaining embryo but the recognizable morphology of the archenteron was re-established. Long after the archenteron reveals territorial specification through expression of specific markers, the endodermal cells remain capable of being respecified to other gut regions. Thus, for much of gastrulation, the gut is conditionally specified. We propose that this regulative ability requires extensive and continuous short-range communication between cells of the archenteron in order to reorganize the tissues and position the boundaries of this structure even after experimental alterations.