Apoptosis is a normal process by which cells die and are eliminated from tissue by phagocytosis [1]. It is involved in regulating cell numbers in adult tissues and in eliminating 'excess' cells during embryogenesis and development. Apoptosis is mediated by activation of caspases, which then cleave a variety of cellular substrates and thereby cause the characteristic morphology of apoptotic cells (rounded cells, condensed chromatin, susceptibility to phagocytosis) [2]. Although apoptosis has been well documented in nematodes, insects and mammals, it is not yet clear how early in evolution apoptosis or its component enzymes arose. In the simple metazoan Hydra vulgaris, cell death regulates cell numbers [3] [4] [5]. In starved animals, for example, epithelial cell proliferation continues at a nearly normal rate although the tissue does not increase in size; the excess cells produced are eliminated by phagocytosis. Cell death can also be induced in wild-type hydra by treatment with colchicine [6] or in a mutant strain (sf-1) by temperature shock [7]. Here, we show that cell death in hydra is morphologically indistinguishable from apoptosis in higher animals, that hydra polyps express two genes with strong homology to members of the caspase 3 family, and that caspase-3-specific enzyme activity accompanies apoptosis in hydra. The occurrence of apoptosis and caspases in a member of the ancient metazoan phylum Cnidaria supports the idea that the invention of apoptosis was an essential feature of the evolution of multicellular animals.

Cnidarians are among the simplest metazoan animals and are well known for their remarkable regeneration capacity. They can regenerate any amputated head or foot, and when dissociated into single cells, even intact animals will regenerate from reaggregates. This extensive regeneration capacity is mediated by epithelial stem cells, and it is based on the restoration of a signaling center, i.e., an organizer. Organizers secrete growth factors that act as long-range regulators in axis formation and cell differentiation. In Hydra, Wnt and TGF-beta/Bmp signaling pathways are transcriptionally up-regulated early during head regeneration and also define the Hydra head organizer created by de novo pattern formation in aggregates. The signaling molecules identified in Cnidarian regeneration also act in early embryogenesis of higher animals. We suppose that they represent a core network of molecular interactions, which could explain at least some of the mechanisms underlying regeneration in vertebrates. Developmental Dynamics 226:257-267, 2003.

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Differentiation of sensory nerve cells in tentacles of Hydra magnipapillata was investigated using the monoclonal antibody NV1. NV1+ sensory nerve cells form specific complexes with battery cells in tentacles. NV1+ cells can only be formed by differentiation from interstitial cell precursors. These precursors complete a terminal cell cycle in the distal gastric region at the base of tentacles; differentiation from the S/G2 boundary to expression of the NV1 antigen requires 30h. During this time, precursors move from the distal gastric region into the tentacles, differentiate to morphologically fully formed nerve cells and then begin expressing NV1 antigen. The neuropeptide head activator stimulates NV1+ differentiation in S-phase of the precursor's cell cycle.

Stimulation of tentacle-specific cell differentiation by the neuropeptide head activator was investigated in Hydra magnipapillata. Tentacle-specific sensory nerve cells were identified by a monoclonal antibody, NV1. Treatment of hydra with 1pM head activator for 18h stimulated differentiation of NV1+ nerve cells and tentacle epithelial cells in tissue from the distal gastric region. Head tissue and tissue from the proximal gastric region did not respond to head activator treatment with increased NV1+ differentiation. Hence the distal gastric region appears to be the site of tentacle formation in hydra. Tentacle precursors in head tissue seem to be committed since they fail to respond to head activator or to changes in tissue size with altered amounts of tentacle formation. We suggest that NV1 precursors form a complex with tentacle epithelial cell precursors, which then moves distally through the head region into the tentacles. The signal for NV1+ differentiation appears to be formation of this complex.

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