SPONGES (PORIFERA) MODEL SYSTEMS TO STUDY THE SHIFT FROM IMMORTAL TO SENESCENT SOMATIC-CELLS - THE TELOMERASE ACTIVITY IN SOMATIC-CELLS

Citation
C. Koziol et al., SPONGES (PORIFERA) MODEL SYSTEMS TO STUDY THE SHIFT FROM IMMORTAL TO SENESCENT SOMATIC-CELLS - THE TELOMERASE ACTIVITY IN SOMATIC-CELLS, Mechanism of ageing and development, 100(2), 1998, pp. 107-120
Citations number
67
Categorie Soggetti
Geiatric & Gerontology",Biology,"Cell Biology
ISSN journal
00476374
Volume
100
Issue
2
Year of publication
1998
Pages
107 - 120
Database
ISI
SICI code
0047-6374(1998)100:2<107:S(MSTS>2.0.ZU;2-8
Abstract
Sponges (Porifera) represent the lowest metazoan phylum, characterized by a pronounced plasticity in the determination of cell lineages. In a first approach to elucidate the molecular mechanisms controlling the switch from the cell lineage with a putative indefinite growth capaci ty to senescent, somatic cells, the activity of the telomerase as an i ndicator for immortality has been determined. The studies were perform ed with the marine demosponges Suberites domuncula and Geodia cydonium . It was found that the activity for the telomerase in the tissue of b oth sponges is high; a quantitative analysis revealed that the extract from S. domuncula contained 10.3 TPG units per 5000 cell equivalents and the one from G. cydonium 8.3 TPG units; hence the activity reached approximately 30-20% of the activity seen in telomerase-positive refe rence cells. In contrast, dissociated spherulous cells from G. cydoniu m, after an incubation period of 24 h, contained no detectable telomer ase activity. From earlier studies it is known that isolated sponge ce lls do not proliferate. Based on these findings it is assumed that the separation of the senescent sponge cell lineage from the immortal ger m/somatic cell lineage is triggered by the loss of contact with cell a dhesion factors. First evidence is included which suggests that the fi nal progress of the senescent, telomerase-negative cells to cell death is caused by apoptosis. (C) 1998 Elsevier Science Ireland Ltd.