Many species of
Tetrahymena are known to display unique response mechanisms to stress and various environmental pressures. The unique genomic architecture of the ciliates (presence of a MIC, high ploidy, large number of chromosomes, etc.) allows for differential gene expression, as well as increased genomic flexibility. The following is a non-exhaustive list of examples of phenotypic and genotypic plasticity in the Tetrahymena genus.
Inducible trophic polymorphisms T. vorax is known for its inducible trophic polymorphisms, an ecologically offensive tactic that allows it to change its feeding strategy and diet by altering its morphology. Normally,
T. vorax is a bacterivorous microstome around 60 μm in length. However, it has the ability to switch into a carnivorous macrostome around 200 μm in length that can feed on larger competitors. If
T. vorax cells are too nutrient starved to undertake transformation, they have also been recorded as transforming into a third "tailed"-microstome morph, thought to be a defense mechanism in response to cannibalistic pressure. While
T. vorax is the most well studied
Tetrahymena that exhibits inducible trophic polymorphisms, many lesser known species are able to undertake transformation as well, including
T. paulina and
T. paravorax. However, only
T. vorax has been recorded as having both a macrostome and tailed-microstome form. These morphological switches are triggered by an abundance of stomatin in the environment, a mixture of metabolic compounds released by competitor species, such as
Paramecium,
Colpidium, and other
Tetrahymena. Specifically, chromatographic analysis has revealed that
ferrous iron,
hypoxanthine, and
uracil are the chemicals in stomatin responsible for triggering the morphological change. Many researchers cite "starvation conditions" as inducing the transformation, as in nature, the compound inducers are in highest concentration after microstomal ciliates have grazed down bacterial populations, and ciliate populations are high. When the chemical inducers are in high concentration,
T. vorax cells will transform at higher rates, allowing them to prey on their former trophic competitors. The exact genetic, and structural mechanisms that underlie
T. vorax transformation are unknown. However, some progress has been made in identifying candidate genes. Researchers from the University of Alabama have used cDNA subtraction to remove actively transcribed DNA from microstome and macrostome
T. vorax cells, leaving only differentially transcribed cDNA molecules. While nine differentiation-specific genes were found, the most frequently expressed candidate gene was identified as a novel sequence,
SUBII-TG. The sequenced region of
SUBII-TG was 912 bp long and consists of three largely identical 105 bp open-reading frames. A northern blot analysis revealed that low levels of transcription are detected in microstome cells, while high levels of transcription occur in macrostome cells. Furthermore, when the researchers limited
SUBII-TG expression in the presence of stomatin (using antisense oligonucleotide methods), a 55% reduction in
SUBII-TG mRNA correlated with a 51% decrease in transformation, supporting the notion that the gene is at least partially responsible for controlling the transformation in
T. vorax. However, very little is known about the
SUBII-TG gene. Researchers were only able to sequence a portion of the entire open-reading frame, and other candidate genes have not been investigated thoroughly. mRNA and amino acid sequencing indicate that ubiquitin may play a crucial role in allowing transformation to take place as well. However, no known genes in the ubiquitin family have been identified in
T. vorax. Finally, the genetic mechanisms of the "tailed" microstome morph are completely unknown.
Metal resistance, gene and genome amplification Other related species exhibit their own unique responses to various stressors. In
T. thermophila, chromosome amplification and gene expansion are inducible responses to common organometallic pollutants such as cadmium, copper, and lead. Strains of
T. thermophila that were exposed to large quantities of Cd2+ over time were found to have a 5-fold increase of
MTT1, and
MTT3 (metallothionein genes that code for Cadmium and Lead binding proteins) as well as
CNBDP, an unrelated gene that lies just upstream of
MTT1 on the same chromosome. The fact that a non-metallothionein gene on the same locus as
MTT1 and
MTT3 increased copy number indicates that the entire chromosome had been amplified, as opposed to just specific genes.
Tetrahymena species are 45-ploid for their macronucleus, meaning that the wild type of
T. thermophila normally contains 45 copies of each chromosome. While the actual number of unique chromosomes are unknown, the number is thought to be around 187 in the MAC, and 5 in the MIC. Thus, the Ca2+ adapted strain contained 225 copies of the specific chromosome in question. This resulted in a nearly 28-fold increase in detected expression levels of
MTT1, and slightly less in
MTT3. When researchers grew a sample of the
T. thermophila population in normal growth medium (lacking Cd2+) for one month, the number of
MTT1,
MTT3, and
CNBDP genes decreased to an average of three copies (135C). By seven months in normal growth medium, the
T. thermophila cells were found reduced to just the wild type copy number (45C). When researchers returned cells from the same colony to Cd2+ medium, within a week
MTT1,
MTT3, and
CNBDP genes increased to three copies once again (135C). Thus, the authors argue that chromosome amplification is an inducible and reversible mechanism in the
Tetrahymena genetic response to metal stress. Researchers also used gene-knockdown experiments, where the copy number of another metallothionein gene on a different chromosome,
MTT5, was dramatically reduced. Within a week, the new strain was found to have developed four novel genes from at least one duplication of
MTT1. However, chromosome duplication had not taken place, as indicated by the wild-type ploidy and the normal quantity of other genes on the same chromosomes. Rather, researchers believe that the duplication resulted from homologous recombination events, producing transcriptionally active, upregulated genes that carry repeated
MTT1.
Enhanced motility and dispersal T. thermophila also undergoes phenotypic changes when faced with limited resource availability. Cells are capable of changing their shape and size, along with behavioral swimming strategies in response to starvation. The more motile cells that change in response to starvation are known as dispersers, or disperser cells. While rates and levels of phenotypic change differ between strains, disperser cells form in nearly all strains of
T. thermophila when faced with starvation. Dispersers, and non-dispersing cells both become dramatically thinner and smaller, increasing the basal body and cilia density, allowing them to swim between two and three times faster than normal cells. Some strains of
T. thermophila have also been found to develop a single, non-beating, enlarged cilia that assists the cell in steering or directing movement. While the behavior has been shown to correlate with faster dispersal and form as a reversible trait in
Tetrahymena cells, little is known about the genetic or cellular mechanisms that allow for its development. Furthermore, other studies show that when genetically variable populations of
T. thermophila were starved, dispersal cells actually increased in cell length, despite still becoming thinner. More research is needed to determine the genetic mechanisms that underlie disperser formation. == Species in genus ==