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Genetic analysis of developmental mechanisms in hydra: XIV. Identification of the cell lineages responsible for the altered developmental gradients in a mutant strain,reg-16
Affiliation:1. Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA;2. Department of Biology, MIT, Cambridge, MA 02139, USA;3. Howard Hughes Medical Institute, MIT, Cambridge, MA 02139, USA;1. Materials and Structural Systems Division, Engineering Laboratory, National Institute of Standards and Technology, Gaithersburg, MD, 20899, USA;2. Materials Science and Engineering Division, Materials Measurement Laboratory, National Institute of Standards and Technology, Gaithersburg, MD, 20899, USA;1. Department of Physical Sciences, P D Patel Institute of Applied Sciences, Charotar University of Science and Technology, CHARUSAT, Changa, 388 421, Gujarat, India;2. AESD&CIF, CSIR-CSMCRI, G B Marg, Waghwadi Road, Bhavnagar, Gujarat, 364002, India;1. Laboratoire B2PE (biologie et pathologie du pancréas endocrine), unité BFA (biologie fonctionnelle et adaptive), CNRS UMR 8251, université Paris-Cité, Paris, France;2. Shandong Institute of Endocrine and Metabolic Diseases ; Shandong First Medical University & Shandong Academy of Medical Sciences, 18877, Jingshi road, 250001 Jinan, Chine;1. Department of Cell Biology, Duke University Medical Center, Durham, NC 27710, USA;2. Regeneration Next, Duke University, Durham, NC 27710, USA;3. Department of Molecular Biology, Massachusetts General Hospital, Boston, MA 02114, USA;4. Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA
Abstract:The developmental gradients of six chimeric strains of hydra produced from a normal strain (105) and a regeneration-deficient strain (reg-16) were analyzed. The reg-16 mutant has been shown to have a lower gradient of head-activation potential and a higher gradient of head-inhibition potential than the normal 105 strain. The chimeric animals consisted of different combinations of the three self-renewing cell lineages found in hydra (the ectodermal and endodermal epithelial cell lineages and the interstitial cell lineage) from each of the parental origins. To identify the cell lineages responsible for the abnormal gradients in reg-16, the head-activation and head-inhibition potentials of these cell lineage chimeras were assayed by lateral transplantation of tissue. The results obtained have provided evidence which indicates that the defect responsible for the low head-activation potential in reg-16 resides in its ectodermal and endodermal epithelial cell lineages, whereas the defect responsible for its high head-inhibition potential resides in its endodermal epithelial and interstitial cell lineages. The cellular localization of these defects is not identical but very similar to the cellular localization of the regenerative defects in reg-16. This finding is consistent with and supports the view that the abnormalities of the developmental gradients are correlated to the reduced head regenerative capacity in reg-16.
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