Unravelling the Role of the F55 Regulator in the Transition from Lysogeny to UV Induction of Sulfolobus Spindle-Shaped Virus 1
Journal article, 2015
ABSTRACT
Sulfolobus spindle-shaped virus 1 represents a model for studying virus-host interaction in harsh environments, and it is so far
the only member of the family Fuselloviridae that shows a UV-inducible life cycle. Although the virus has been extensively studied,
mechanisms underpinning the maintenance of lysogeny as well as those regulating the UV induction have received little attention.
Recently, a novel SSV1 transcription factor, F55, was identified. This factor was able to bind in vitro to several sequences
derived from the early and UV-inducible promoters of the SSV1 genome. The location of these binding sites together with the
differential affinity of F55 for these sequences led to the hypothesis that this protein might be involved in the maintenance of the
SSV1 lysogeny. Here, we report an in vivo survey of the molecular events occurring at the UV-inducible region of the SSV1 genome,
with a focus on the binding profile of F55 before and after the UV irradiation. The binding of F55 to the target promoters
correlates with transcription repression, whereas its dissociation is paralleled by transcription activation. Therefore, we propose
that F55 acts as a molecular switch for the transcriptional regulation of the early viral genes.
IMPORTANCE
Functional genomic studies of SSV1 proteins have been hindered by the lack of similarity with other characterized proteins. As a
result, few insights into their in vivo roles have been gained throughout the last 3 decades. Here, we report the first in vivo investigation
of an SSV1 transcription regulator, F55, that plays a key role in the transition from the lysogenic to the induced state of
SSV1. We show that F55 regulates the expression of the UV-inducible as well as the early genes. Moreover, the differential affinity
of this transcription factor for these targets allows a fine-tuned and temporal coordinated regulation of transcription of viral
genes.