Genetic analysis of developmental mechanisms in hydra

Development ◽  
1984 ◽  
Vol 80 (1) ◽  
pp. 155-173
Author(s):  
Jun Takano ◽  
Tsutomu Sugiyama
Keyword(s):  
Epithelial Cell ◽  
Interstitial Cell ◽  
Cell Lineage ◽  
Normal Strain ◽  
Polyp Size ◽  
Bud Formation ◽  
Cell Lineages ◽  
Large Polyp ◽  
Naturally Occurring ◽  
High Head

Chimaeric hydra strains were produced from a normal strain (105) and a naturally-occurring mutant strain (L4) which has a large polyp size, a low budding rate and a high head-inhibition potential. Various properties of the chimaeras were then examined and compared to those of the two parental strains. Hydra tissue consists of three cell lineages: the ectodermal epithelial, the endodermal epithelial and the interstitial cell lineages. Using the methods recently developed by Marcum & Campbell (1978b) and by Wanek & Campbell (1982), six chimaeric strains were produced which contained six different combinations of the three cell lineages from 105 and L4. Evidence obtained from the comparison of the chimaeras and their parental strains indicates that the ectodermal epithelial cell lineage in L4 is primarily responsible for the large polyp size and the low budding rate of this strain, whereas the endodermal epithelial cell lineage is largely, and the interstitial cell lineage is also partially, responsible for the high head-inhibition potential in L4. This suggests that the mechanisms determining the occurrence and location of bud formation and the mechanisms determining the inhibition potential levels are not related to each other (cf. Takano & Sugiyama, 1983; Bode & Bode, 1983). Evidence was also obtained which suggests that the levels of the head-activation and head-inhibition potentials in the chimaeras are determined independent of each other, apparently without the cross-catalytic relationship between them assumed in the Gierer-Meinhardt model (Gierer & Meinhardt, 1972; Meinhardt & Gierer, 1974).

Genetic analysis of developmental mechanisms in hydra. V. Cell lineage and development of chimera hydra

1978 ◽  
Vol 32 (1) ◽  
pp. 215-232
Author(s):  
T. Sugiyama ◽  
T. Fujisawa
Keyword(s):  
Epithelial Cell ◽  
Epithelial Cells ◽  
Interstitial Cell ◽  
Cell Lineage ◽  
Interstitial Cells ◽  
Nerve Cells ◽  
Polyp Size ◽  
Primary Determinant ◽  
One Year ◽  
Almost All

Chimeric hydra were produced by making use of a strain (nf-1) which lacks interstitial cells, nerve cells and nematocytes. This strain arises by spontaneous loss of interstitial cells from its parental strain (sf-1) (Sugiyama & Fujisawa, 1978). Reintroduction of interstitial cells from other strains into nf-1 leads to the creation of chimeric strains that consisted of epithelial cells derived from strain sf-1 and interstitial cells and their derivatives (nerves and nematocytes) from other strains. In chimeras, interstitial or epithelial cells apparently maintain very stable cell lineages; no indication was obtained that suggested interstitial cell differentiation into epithelial cells or dedifferentiation in the opposite direction during the long courses of chimera cultures (up to one year). Developmental characters of chimeras were examined and compared to those of the epithelial cell (sf-1) and the interstitial cell donors. Almost all of the chimera's characters examined (growth rate, budding rate, tentacle numbers, polyp size, regenerative capacity, etc.) closely resembled those of the epithelial cell donor, but not of the interstitial cell donors. This suggests that epithelial cells, rather than interstitial or nerve cells, are the primary determinant of most, if not all, of hydra developmental characters.

Lectins are sensitive tools for defining the differentiation programs of mouse gut epithelial cell lineages

1994 ◽  
Vol 266 (6) ◽  
pp. G987-G1003 ◽  
Author(s):  
P. Falk ◽  
K. A. Roth ◽  
J. I. Gordon
Keyword(s):  
Epithelial Cell ◽  
Transgenic Mice ◽  
Intestinal Epithelial Cell ◽  
Cell Lineage ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
T Antigen ◽  
Intestinal Epithelial ◽  
Cell Lineages ◽  
Carbohydrate Specificities

We have used histochemical methods to survey the cellular patterns of binding of a panel of 45 lectins with well-defined carbohydrate specificities to sections prepared from various regions of the gastric-to-colonic axis of fetal, neonatal, and adult FVB/N mouse gut. The results suggest that lectins can be used as remarkably sensitive tools to describe the differentiation programs of gastric and intestinal epithelial cell lineages as a function of their position along the cephalocaudal axis of the gut and as a function of developmental stage. Studies of intestinal isografts and transgenic mice that express Simian virus-40 T antigen in enterocytes suggest that many of these cell lineage-specific and spatial patterns of glycoconjugate production can be established and maintained in the absence of exposure to luminal contents and in the presence of specific proliferative abnormalities. This lectin panel should be useful for operationally defining subpopulations of the principal gut epithelial cell lineages in normal strains of mice, for describing variations in gut epithelial cell differentiation programs in mutant and transgenic mice, and for recovering specific epithelial cell lineages or subpopulations.

Developmental roles of epithelial and interstitial cell lineages in hydra: analysis of chimeras

1978 ◽  
Vol 32 (1) ◽  
pp. 233-247
Author(s):  
B.A. Marcum ◽  
R.D. Campbell
Keyword(s):  
Epithelial Cell ◽  
Epithelial Cells ◽  
Interstitial Cell ◽  
Interstitial Cells ◽  
Considerable Influence ◽  
Cell Lineages

Chimeric hydra were prepared by recombining epithelial and interstitial cells between 3 strains of hydra of different sizes (maxi, normal, and mini strains). The resulting chimeras generally resembled the epithelial cell parent more than the interstitial cell parent in size, budding rate, tentacle number, and form. This suggests that epithelial cells normally exert considerable influence over hydra morphogenesis. However, the chimeras show some differences ascribable to interstitial cell origin. Furthermore, the 3 original strains, when deprived of interstitial cells, lose their distinguishing size differences. Thus both epithelial and interstitial cells (or interstitial cell derivatives) mutually participate in hydra's development.

Genetic analysis of developmental mechanisms in hydra. VI. Cellular composition of chimera hydra

1979 ◽  
Vol 35 (1) ◽  
pp. 1-15
Author(s):  
T. Sugiyama ◽  
T. Fujisawa
Keyword(s):  
Epithelial Cell ◽  
Genetic Analysis ◽  
Interstitial Cell ◽  
Cell Types ◽  
Interstitial Cells ◽  
Cellular Composition ◽  
Feedback Mechanisms ◽  
Cell Lineages ◽  
Developmental Mechanisms ◽  
Homeostatic Mechanisms

The homeostatic mechanisms that maintain constant cellular ratios in hydra tissue were studied using mutant and chimeric hydra strains. Mutants having abnormal cellular compositions are isolated through sexual inbreeding of wild hydra, as described in previous papers of this series. Chimeric hydra are produced by making use of a strain (nf-I) which lacks interstitial cells, nerve cells and nematocytes in its tissue. Reintroduction of interstitial cells from other strains (both normal and mutant) into nf-I leads to creation of chimeric strains having epithelial cell lineages from one strain (nf-I) and interstitial cell lineages from others. Analyses and comparisons of the cellular compositions of all these strains revealed that the numbers of nerve or interstitial cells in the chimeras were very similar to (statistically significantly correlated with) those in their interstitial cell donors. Since chimeras and their interstitial cell donors share the same interstitial cell lineages, this suggests that interstitial cells or their derivatives (nerves and nematocytes) play major roles in determining the nerve and interstitial cell levels in the hydra tissue. It is suggested that some form of homeostatic feedback mechanisms are probably involved in regulating the levels of these cell types.

scholarly journals A second transmissible cancer in Tasmanian devils

2015 ◽  
Vol 113 (2) ◽  
pp. 374-379 ◽  
Author(s):  
Ruth J. Pye ◽  
David Pemberton ◽  
Cesar Tovar ◽  
Jose M. C. Tubio ◽  
Karen A. Dun ◽  
...  
Keyword(s):  
Major Histocompatibility Complex ◽  
Cancer Cells ◽  
Cell Lineage ◽  
Tasmanian Devil ◽  
Second Cancer ◽  
Cell Lineages ◽  
Histocompatibility Complex ◽  
Naturally Occurring ◽  
Soft Shell ◽  
Transmissible Cancer

Clonally transmissible cancers are somatic cell lineages that are spread between individuals via the transfer of living cancer cells. There are only three known naturally occurring transmissible cancers, and these affect dogs, soft-shell clams, and Tasmanian devils, respectively. The Tasmanian devil transmissible facial cancer was first observed in 1996, and is threatening its host species with extinction. Until now, this disease has been consistently associated with a single aneuploid cancer cell lineage that we refer to as DFT1. Here we describe a second transmissible cancer, DFT2, in five devils located in southern Tasmania in 2014 and 2015. DFT2 causes facial tumors that are grossly indistinguishable but histologically distinct from those caused by DFT1. DFT2 bears no detectable cytogenetic similarity to DFT1 and carries a Y chromosome, which contrasts with the female origin of DFT1. DFT2 shows different alleles to both its hosts and DFT1 at microsatellite, structural variant, and major histocompatibility complex (MHC) loci, confirming that it is a second cancer that can be transmitted between devils as an allogeneic, MHC-discordant graft. These findings indicate that Tasmanian devils have spawned at least two distinct transmissible cancer lineages and suggest that transmissible cancers may arise more frequently in nature than previously considered. The discovery of DFT2 presents important challenges for the conservation of Tasmanian devils and raises the possibility that this species is particularly prone to the emergence of transmissible cancers. More generally, our findings highlight the potential for cancer cells to depart from their hosts and become dangerous transmissible pathogens.

scholarly journals Aspects of the biology of regeneration and repair in the human gastrointestinal tract

1998 ◽  
Vol 353 (1370) ◽  
pp. 925-933 ◽  
Author(s):  
Nicholas A. Wright
Keyword(s):  
Stem Cells ◽  
Gastric Gland ◽  
Cell Lineage ◽  
Mucosal Ulceration ◽  
Cell Lineages ◽  
Trefoil Peptides ◽  
Pyloric Mucosa ◽  
A Cell ◽  
Epidermal Growth ◽  
Altered Gene

The main pathways of epithelial differentiation in the intestine, Paneth, mucous, endocrine and columnar cell lineages are well recognized. However, in abnormal circumstances, for example in mucosal ulceration, a cell lineage with features distinct from these emerges, which has often been dismissed in the past as ‘pyloric’ metaplasia, because of its morphological resemblance to the pyloric mucosa in the stomach. However, we can conclude that this cell lineage has a defined phenotype unique in gastrointestinal epithelia, has a histogenesis that resembles that of Brunner's glands, but acquires a proliferative organization similar to that of the gastric gland. It expresses several peptides of particular interest, including epidermal growth factor, the trefoil peptides TFF1, TFF2, TFF3, lysozyme and PSTI. The presence of this lineage also appears to cause altered gene expression in adjacent indigenous cell lineages. We propose that this cell lineage is induced in gastrointestinal stem cells as a result of chronic mucosal ulceration, and plays an important part in ulcer healing; it should therefore be added to the repertoire of gastrointestinal stem cells.

ISOLATION AND GENETIC CHARACTERIZATION OF CELL-LINEAGE MUTANTS OF THE NEMATODE CAENORHABDITIS ELEGANS

Genetics ◽  
1980 ◽  
Vol 96 (2) ◽  
pp. 435-454 ◽  
Author(s):  
H Robert Horvitz ◽  
John E Sulston
Keyword(s):  
Caenorhabditis Elegans ◽  
Cell Lineage ◽  
Embryonic Cell ◽  
Null Alleles ◽  
Recessive Mutation ◽  
Incomplete Penetrance ◽  
Nematode Caenorhabditis Elegans ◽  
Cell Lineages ◽  
Cell Divisions ◽  
Recessive Mutations

ABSTRACT Twenty-four mutants that alter the normally invariant post-embryonic cell lineages of the nematode Caenorhabditis elegans have been isolated and genetically characterized. In some of these mutants, cell divisions fail that occur in wild-type animals; in other mutants, cells divide that do not normally do so. The mutants differ in the specificities of their defects, so that it is possible to identify mutations that affect some cell lineages but not others. These mutants define 14 complementation groups, which have been mapped. The abnormal phenotype of most of the cell-lineage mutants results from a single recessive mutation; however, the excessive cell divisions characteristic of one strain, CB1322, require the presence of two unlinked recessive mutations. All 24 cell-lineage mutants display incomplete penetrance and/or variable expressivity. Three of the mutants are suppressed by pleiotropic suppressors believed to be specific for null alleles, suggesting that their phenotypes result from the complete absence of gene activity.

ming is expressed in neuroblast sublineages and regulates gene expression in the Drosophila central nervous system

Development ◽  
1992 ◽  
Vol 116 (4) ◽  
pp. 943-952 ◽  
Author(s):  
X. Cui ◽  
C.Q. Doe
Keyword(s):  
Gene Expression ◽  
Central Nervous System ◽  
Nervous System ◽  
Cell Fate ◽  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Cell Lineage ◽  
Cell Lineages ◽  
Finger Protein ◽  
Cell Diversity

Cell diversity in the Drosophila central nervous system (CNS) is primarily generated by the invariant lineage of neural precursors called neuroblasts. We used an enhancer trap screen to identify the ming gene, which is transiently expressed in a subset of neuroblasts at reproducible points in their cell lineage (i.e. in neuroblast ‘sublineages’), suggesting that neuroblast identity can be altered during its cell lineage. ming encodes a predicted zinc finger protein and loss of ming function results in precise alterations in CNS gene expression, defects in axonogenesis and embryonic lethality. We propose that ming controls cell fate within neuroblast cell lineages.

scholarly journals Early developmental asymmetries in cell lineage trees in living individuals

2020 ◽  
Author(s):  
Liana Fasching ◽  
Yeongjun Jang ◽  
Simone Tomasi ◽  
Jeremy Schreiner ◽  
Livia Tomasini ◽  
...  
Keyword(s):  
Cell Fate ◽  
Cell Lineage ◽  
Postmortem Brain ◽  
Cell Lineages ◽  
Human Specimen ◽  
Balanced Contributions ◽  
Health And Disease ◽  
Induced Pluripotent ◽  
Lineage Trees ◽  
Early Developmental

AbstractPost-zygotic mosaic mutations can be used to track cell lineages in humans. By using cell cloning and induced pluripotent cell lines, we analyzed early cell lineages in two living individuals (a patient and a control), and a postmortem human specimen. Of ten reconstructed post-zygotic divisions, none resulted in balanced contributions of daughter lineages to tissues. In both living individuals one of two lineages from the first cleavage was dominant across tissues, with 90% frequency in blood. We propose that the efficiency of DNA repair contributes to lineage imbalance. Allocation of lineages in postmortem brain correlated with anterior-posterior axis, associating lineage history with cell fate choices in embryos. Recurrence of germline variants as mosaic suggested that certain loci may be particularly susceptible to mutagenesis. We establish a minimally invasive framework for defining cell lineages in any living individual, which paves the way for studying their relevance in health and disease.

scholarly journals The proportion of mitoses in different cell lineages changes during short-term culture of normal human bone marrow

Blood ◽  
1986 ◽  
Vol 67 (5) ◽  
pp. 1240-1243
Author(s):  
M Keinanen ◽  
S Knuutila ◽  
CD Bloomfield ◽  
E Elonen ◽  
A de la Chapelle
Keyword(s):  
Bone Marrow ◽  
Cell Lineage ◽  
Great Majority ◽  
Hematopoietic Cell ◽  
Human Bone ◽  
Human Bone Marrow ◽  
Immunofluorescent Staining ◽  
Cytoplasmic Staining ◽  
Cell Lineages ◽  
Mitotic Cells

To determine the hematopoietic cell lineage of mitotic cells in human bone marrow on direct examination and after 24-hour culture, marrow mitoses from four healthy individuals were studied, using a new technique that allows analysis of karyotypes in cells whose cell membrane and cytoplasm have been preserved. Mitoses were identified as being of erythroid lineage by immunofluorescent staining for surface glycophorin A and as being of granulocytic lineage by cytoplasmic staining for Sudan black B. On direct marrow examination without prior culture, the great majority of mitoses (74% to 90%) were of erythroid lineage; only a few (0% to 10%) were granulocytic. After 24-hour culture, the percentage of erythroid mitoses (15% to 40%) decreased, while the percentage of granulocytic mitoses (58% to 87%) increased strikingly. These data indicate that mitotic cells of different hematopoietic cell lineages predominate in marrow at different culture times and offer a plausible explanation for the high frequency of normal karyotypes in acute myeloid leukemia after direct marrow cytogenetic evaluation.

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