TbsP and TrmB jointly regulate gapII to influence cell development
phenotypes in the archaeon Haloferax volcanii
Abstract
Microbial cells must continually adapt their physiology in the face of
changing environmental conditions. Archaea living in extreme conditions,
such as saturated salinity, represent important examples of such
resilience. The model salt-loving organism Haloferax volcanii
exhibits remarkable plasticity in its morphology, biofilm formation, and
motility in response to variations in nutrients and cell density.
However, the mechanisms regulating these lifestyle transitions remain
unclear. In prior research, we showed that the transcriptional
regulator, TrmB, maintains the rod shape in the related species
Halobacterium salinarum by activating the expression of
enzyme-coding genes in the gluconeogenesis metabolic pathway. In
Hbt. salinarum, TrmB-dependent production of glucose moieties is
required for cell surface glycoprotein biogenesis. Here we use a
combination of genetics, quantitative phenotyping, and gene expression
assays to demonstrate that TrmB is essential for growth under
gluconeogenic conditions in Hfx. volcanii. The ∆ trmB
strain rapidly accumulated suppressor mutations in a gene encoding a
novel transcriptional regulator, which we name Trm B
su ppressor, or TbsP. TbsP is required for adhesion to
abiotic surfaces (i.e. biofilm formation), and maintains wild type cell
morphology, and motility. TrmB and TbsP jointly regulate the
glucose-dependent transcription of gapII, which encodes an
important gluconeogenic enzyme. We conclude that TrmB and TbsP
co-regulate gluconeogenesis, with downstream impacts on lifestyle
transitions in response to nutrients in Hfx. volcanii.