scholarly journals Elimination by Hydra interstitial and nerve cells by means of colchicine

1976 ◽  
Vol 21 (1) ◽  
pp. 1-13 ◽  
Author(s):  
R.D. Campbell

Hydra treated with colchicine or Colcemid become depleted of 95–99% of their interstitial cells and derivatives of this stem cell: nematoblasts, nematocytes and nerve cells. A second treatment removes most or all remaining interstitial cells. The most effective treatment is an 8-h immersion of whole Hydra attenuata in 0.04% Colcemid or 0.4% colchicine. Interstitial cells are eliminated through phagocytosis by both ectodermal and endodermal epithelial cells. The endodermal digestive cells send processes through the mesoglea which engulf interstitial cells and retract them into the endoderm. The resultant hydra, though devoid of nematocysts, can be artificially fed: these animals grow and bud and can be used to study the behaviour and development of tissue lacking nerve and interstitial cells.

1974 ◽  
Vol 16 (2) ◽  
pp. 359-375 ◽  
Author(s):  
C. N. DAVID ◽  
A. GIERER

The differentiation of nerve cells and nematocytes in Hydra attenuata has been investigated by labelling interstitial cell precursors with [3H]thymidine and following by autoradiography the appearance of labelled, newly differentiated cells. Nematocyte differentiation occurs only in the gastric region where labelled nematoblasts appear 12 h and labelled nematocytes 72-96 h after addition of [3H]thymidine. Labelled nerves appear in hypostome, gastric region, and basal disk about 18 h after addition of [3H]thymidine. The lag in the appearance of labelled cells includes cell division of the precursor as well as differentiation since nerves and nematocytes have 2n postmitotic nuclear DNA content. A cell flow model is proposed for interstitial cells and their differentiated products. Stem cells occur as single interstitial cells or in pairs. Per cell generation about 60 % of the daughter cells of stem cell divisions remain stem cells and about 40 % differentiate nerves and nematocytes. Nerves differentiate directly from stem cells in about 1 day. Nematocyte differentiation requires 5-7 days including proliferation of a cluster of 4, 8, 16 or 32 interstitial cells and differentiation of a nematocyst capsule in each cell. The numbers of interstitial cells and nematoblasts predicted by the cell flow model from the rates of nerve differentiation (900 nerves/day/ hydra), nematocyte differentiation (1760 nematocyte nests/day/hydra) and stem cell proliferation (stem cell cycle = 24 h), agree with the numbers of these cells observed in hydra. The number of stem cells per hydra is 3000-6000 depending on assumptions about the time of determination. The ratio of nematocyte to nerve differentiation averaged over the whole hydra is 3:1. In the hypostome and basal disk interstitial cell differentiation occurs exclusively to nerve cells while in the gastric region the ratio of nematocyte to nerve differentiation is about 7:1.


1978 ◽  
Vol 32 (1) ◽  
pp. 215-232
Author(s):  
T. Sugiyama ◽  
T. Fujisawa

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.


Development ◽  
1977 ◽  
Vol 42 (1) ◽  
pp. 65-77
Author(s):  
Tsutomu Sugiyama ◽  
Toshitaka Fujisawa

Mutant hydra strains showing abnormal development can be isolated through sexual inbreeding of wild hydra. One such mutant strain, called reg-16, regenerates tentacles very poorly following amputation of the head and foot. Tentacle regeneration, however, is significantly enhanced by subdividing the regenerating fragment longitudinally. Lateral tissue implants that induce head formation in wild-type hydra either regress or induce foot formation in reg-16 polyps. These results suggest that regeneration deficiency in reg-16 is due to a defective polarity gradient. A chimaeric strain of hydra was produced by combining interstitial cells (and thus their differentiation products, nerve cells and nematocytes) of reg-16 hydra with epithelial cells of another strain which is capable of normal regeneration. The chimaeras regenerate normally, suggesting that the defect of reg-16 is not located in the interstitial or nerve cells.


1978 ◽  
Vol 34 (1) ◽  
pp. 27-38
Author(s):  
M.S. Yaross ◽  
H.R. Bode

In hydra, nerve cells are a differentiation product of the interstitial cell, a multipotent stem cell. Nerve cell commitment was examined during head regeneration in Hydra attenuata. Within 3 h of head removal there is a 10- to 20-fold increase in nerve cell commitment in the tissue which subsequently forms the new head. Nerve cell commitment is unaltered in the remainder of the gastric region. This local increase in nerve cell commitment is responsible for about one half the new nerve cells formed during head regeneration, while one half differentiate from interstitial cells that migrate into the regenerating tip.


1998 ◽  
Vol 76 (6) ◽  
pp. 1069-1077 ◽  
Author(s):  
Cheng-Ming Chuong ◽  
Han-Sung Jung ◽  
Drew Noden ◽  
Randall B Widelitz

How do epithelial cells in developing skin accommodate the constantly growing embryo? Where do cells in skin appendages come from? Are they derivatives of a single appendage stem cell, or are they polyclonal? Here we analyze these issues in developing chicken skin using a replication-defective virus carrying beta-galactosidase and DiI microinjections. The results demonstrate that in early skin, epithelial cells labelled near the spine show a parallel linear stripe distribution pattern that is perpendicular to the midline of the trunk. This is similar to the human lines of Blaschko, a linear pattern on the skin, which many skin nevoid or acquired disorders follow. In later skin, feather buds form and contain a mixture of labeled and unlabeled cells, attesting to their polyclonal origin. When cells are traced for shorter time intervals, the labeled progeny appear to follow certain rules. The degree of cell dispersion and mixing increases with a longer incubation period between the time of labeling and detection. The spatial maturation sequence of skin appendages is not regulated by the order in which epithelial cells are generated. Epithelial cells at this developmental stage are pluripotent and competent to respond to new signals to assume appropriate fates according to their micro-environment. The results suggest that local interactions act upon the originally linearly deposited pluripotential epithelial cells to form skin appendages.Key words: cell lineage, organogenesis, stem cell, skin appendages, feather, hair.


2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Patrick D. Rädler ◽  
Barbara L. Wehde ◽  
Aleata A. Triplett ◽  
Hridaya Shrestha ◽  
Jonathan H. Shepherd ◽  
...  

AbstractClaudin-low breast cancer represents an aggressive molecular subtype that is comprised of mostly triple-negative mammary tumor cells that possess stem cell-like and mesenchymal features. Little is known about the cellular origin and oncogenic drivers that promote claudin-low breast cancer. In this study, we show that persistent oncogenic RAS signaling causes highly metastatic triple-negative mammary tumors in mice. More importantly, the activation of endogenous mutant KRAS and expression of exogenous KRAS specifically in luminal epithelial cells in a continuous and differentiation stage-independent manner induces preneoplastic lesions that evolve into basal-like and claudin-low mammary cancers. Further investigations demonstrate that the continuous signaling of oncogenic RAS, as well as regulators of EMT, play a crucial role in the cellular plasticity and maintenance of the mesenchymal and stem cell characteristics of claudin-low mammary cancer cells.


PLoS ONE ◽  
2011 ◽  
Vol 6 (12) ◽  
pp. e29007 ◽  
Author(s):  
Jonathan Ferrand ◽  
Philippe Lehours ◽  
Annie Schmid-Alliana ◽  
Francis Mégraud ◽  
Christine Varon

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