Transmissible Tumors in Hydra Oligactis Can Manipulate Host Phenotype by Inducing Supernumerary Tentacles

Core Concepts

Transmissible tumors in Hydra oligactis can manipulate the host phenotype by inducing the growth of additional tentacles, which enhances the vertical transmission of the tumors.

Abstract

The study explores whether transmissible tumors in the cnidarian Hydra oligactis can manipulate the phenotype of their host, as observed in many parasites. The researchers found that hydras with long-term transmissible tumors show an increased number of tentacles compared to healthy hydras or those with spontaneous tumors.
Through a series of tissue transplantation experiments, the authors demonstrate that only the transmissible tumors, and not spontaneous tumors, are able to trigger the growth of additional tentacles in the recipient hydras. This phenotypic change appears to be an adaptation that enhances the vertical transmission of the tumors, as the increased number of tentacles is associated with higher prey capture and budding rates.
In contrast, spontaneous tumors that lack a long evolutionary history with the host do not induce this phenotypic manipulation. The results provide the first evidence that, like true parasites, transmissible tumor cells can evolve strategies to manipulate the phenotype of their host to favor their own transmission.
The authors also report an unexpected finding that healthy tissue grafts can sometimes lead to the development of new tumors in the recipient hydras, suggesting the host's ability to control abnormal cell proliferation can be weakened by the transplantation process.

Stats

Hydras with transmissible tumors typically have 8-13 tentacles, while healthy hydras and those with spontaneous tumors have 6-7 tentacles.
Hydras grafted with transmissible tumor tissues developed on average 8 times more tumors than those grafted with healthy tissues.
Hydras grafted with transmissible tumor tissues developed on average 1.45 additional tentacles, while those grafted with healthy tissues developed only 1 additional tentacle.
The number of buds produced per individual was significantly correlated with the number of supernumerary tentacles developed, but this correlation was reduced for hydras with tumors.

Quotes

"Remarkably, the hydras with long-term transmissible tumors show an unexpected increase in the number of their tentacles, allowing for the possibility that these neoplastic cells can manipulate the host."
"To our knowledge, this is the first evidence that, like true parasites, transmissible tumors can evolve strategies to manipulate the phenotype of their host."
"Transmissible tumors propagated in the laboratory for more than 10 years can induce the growth of additional tentacles even when they are transplanted in new hosts."

Key Insights Distilled From

First evidence for the evolution of host manipulation by tumors during the long-term vertical transmission of tumor cells in Hydra oligactis

by BOUTRY,J., O... at www.biorxiv.org 02-09-2024

https://www.biorxiv.org/content/10.1101/2024.02.08.579507v1

Deeper Inquiries

What are the specific molecular and physiological mechanisms by which transmissible tumors in Hydra induce the growth of supernumerary tentacles?

Transmissible tumors in Hydra induce the growth of supernumerary tentacles through complex molecular and physiological mechanisms. One key aspect is the interaction between the tumor cells and the host's signaling pathways. Tumor cells can secrete various growth factors and cytokines that influence the host's cellular processes, leading to the formation of additional tentacles. For example, these tumor-derived factors may activate signaling pathways involved in cell proliferation and tissue regeneration, promoting the development of extra tentacles.
Moreover, the tumor cells may also modulate the host's immune response and inflammatory pathways. By evading immune surveillance or altering the local immune environment, the tumor cells can create a more favorable microenvironment for their growth and induce changes in the host's phenotype, such as the formation of supernumerary tentacles. Additionally, the tumor cells may interact with the host's microbiome, influencing the composition of the microbial community and affecting host physiology.
At the molecular level, the tumor cells likely exhibit genetic and epigenetic alterations that drive their ability to manipulate the host phenotype. These alterations may affect gene expression patterns, leading to changes in cell behavior, tissue morphology, and organ development. By exploiting these molecular mechanisms, transmissible tumors in Hydra can effectively induce the growth of supernumerary tentacles and manipulate the host's phenotype to enhance their own transmission and survival.

How common is the ability of transmissible cancers to manipulate host phenotypes across different species, and what are the evolutionary implications of this phenomenon?

The ability of transmissible cancers to manipulate host phenotypes is relatively rare but has been observed in certain species, such as the Tasmanian devil and Hydra. While most cancers do not exhibit this level of host manipulation, transmissible cancers that can be horizontally or vertically transmitted have a higher likelihood of evolving manipulative abilities. These cancers have a longer evolutionary history with their hosts, allowing them to adapt and develop strategies to influence host phenotypes for their own benefit.
The evolutionary implications of transmissible cancers manipulating host phenotypes are significant. By altering host behavior, morphology, or physiology, these cancers can enhance their transmission and survival, ultimately increasing their evolutionary success. This phenomenon highlights the dynamic and intricate interactions between hosts and parasites, demonstrating the potential for parasites, including cancer cells, to shape the evolution of their hosts.
From an evolutionary perspective, the ability of transmissible cancers to manipulate host phenotypes raises intriguing questions about the coevolutionary dynamics between hosts and parasites. It underscores the importance of understanding the mechanisms underlying host-parasite interactions and the potential impact of parasitic manipulation on host fitness and evolutionary trajectories. Studying transmissible cancers and their effects on host phenotypes can provide valuable insights into the evolutionary arms race between hosts and parasites.

Could the unexpected development of new tumors following healthy tissue grafts in Hydra provide insights into the role of the host's microbiome and immune system in controlling cancer initiation and progression?

The unexpected development of new tumors following healthy tissue grafts in Hydra offers valuable insights into the role of the host's microbiome and immune system in controlling cancer initiation and progression. This phenomenon suggests that the host's immune response and microbiome play crucial roles in regulating tumor development and growth.
The development of tumors in response to tissue grafts may indicate a breakdown in immune surveillance or an imbalance in the host's microbiome, creating a permissive environment for tumor initiation. The host's immune system is responsible for detecting and eliminating abnormal cells, including potentially cancerous ones. When the immune response is compromised or dysregulated, as seen in the context of tissue grafts, it can lead to the unchecked proliferation of tumor cells.
Similarly, the host's microbiome, which consists of diverse microbial communities, can influence immune function and overall health. Disruptions in the microbiome composition or function may impact the host's ability to control tumor growth and progression. The unexpected development of new tumors following healthy tissue grafts in Hydra underscores the intricate interplay between the host's immune system, microbiome, and cancer development.
Studying this phenomenon in Hydra can provide insights into the mechanisms by which the host's immune system and microbiome interact with tumor cells and influence cancer progression. By elucidating the roles of these factors in controlling cancer initiation and progression, researchers can gain a better understanding of how to harness the host's natural defenses to combat cancer and develop novel therapeutic strategies.