Cnephaeus
Ontology highlight
ABSTRACT:
PROVIDER: PRJDB12273 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| DRR318494_1.fastq.gz | Fastqsanger.gz | |||
| DRR318494_2.fastq.gz | Fastqsanger.gz | |||
| DRR318495_1.fastq.gz | Fastqsanger.gz | |||
| DRR318495_2.fastq.gz | Fastqsanger.gz | |||
| DRR318496_1.fastq.gz | Fastqsanger.gz |
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Project description:Bats are remarkably long-lived for their size with many species living more than 20-40 years, suggesting that they possess efficient anti-aging and anti-cancer defenses. Here we investigated requirements for malignant transformation in primary bat fibroblasts in four bat species - little brown bat (Myotis lucifugus), big brown bat (Eptesicus fuscus), cave nectar bat (Eonycteris spelaea) and Jamaican fruit bat (Artibeus jamaicensis) – spanning the bat evolutionary tree and including the longest-lived genera. We show that bat fibroblasts do not undergo replicative senescence and express active telomerase. Bat cells displayed attenuated stress induced premature senescence with a dampened secretory phenotype. Unexpectedly, we discovered that bat cells could be readily transformed by only two oncogenic perturbations or “hits”: inactivation of either p53 or pRb and activation of oncogenic RASV12. This was surprising because other long-lived mammalian species require up to five hits for malignant transformation. Additionally, bat fibroblasts exhibited increased p53 and MDM2 transcript levels, and elevated p53-dependent apoptosis. The little brown bat showed a genomic duplication of the p53 gene. We hypothesize that bats evolved enhanced p53 activity through gene duplications and transcriptional upregulation as an additional anti-cancer strategy, similar to elephants. In summary, active telomerase and the small number of oncogenic hits sufficient to malignantly transform bat cells suggest that in vivo bats rely heavily on non-cell autonomous mechanisms of tumor suppression.
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Project description:Vesper bats (family Vespertilionidae) experienced a rapid adaptive radiation beginning around 36 mya that resulted in the second most species rich mammalian family. Coincident with that radiation was an initial burst of DNA transposon activity that has continued into the present. Deep sequencing of small RNAs from the vespertilionid, Eptesicus fuscus, as well as dog and horse revealed that substantial numbers of novel bat miRNAs are derived from DNA transposons unique to vespertilionids. In fact, 35.9% of Eptesicus-specific miRNAs derive from DNA transposons compared to 2.2 and 5.9% of dog- and horse-specific miRNAs, respectively and targets of several miRNAs are identifiable. Timing of the DNA transposon expansion and the introduction of novel miRNAs coincides remarkably well with the rapid diversification of the family Vespertilionidae. We suggest that the rapid and repeated perturbation of regulatory networks by the introduction of many novel miRNA loci was a factor in the rapid radiation.
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