Salactin, a dynamically unstable actin homolog in Haloarchaea

Jenny Zheng, J. Mallon, Alex Lammers, T. Rados, T. Litschel, E.R.R. Moody, D.A. Ramirez-Diaz, Amy Schmid, T.A. Williams, A.W. Bisson-Filho, E. Garner

Research output: Contribution to journalArticlepeer-review

6 Citations (SciVal)

Abstract

Across the domains of life, actin homologs are integral components of many essential processes, such as DNA segregation, cell division, and cell shape determination. Archaeal genomes, like those of bacteria and eukaryotes, also encode actin homologs, but much less is known about these proteins’ in vivo dynamics and cellular functions. We identified and characterized the function and dynamics of Salactin, an actin homolog in the hypersaline archaeon Halobacterium salinarum. Live-cell time-lapse imaging revealed that Salactin forms dynamically unstable filaments that grow and shrink out of the cell poles. Like other dynamically unstable polymers, Salactin monomers are added at the growing filament end, and its ATP-bound critical concentration is substantially lower than the ADP-bound form. When H. salinarum’s chromosomal copy number becomes limiting under low-phosphate growth conditions, cells lacking Salactin show perturbed DNA distributions. Taken together, we propose that Salactin is part of a previously unknown chromosomal segregation apparatus required during low-ploidy conditions.
Original languageEnglish
Article numbere02272-23
Number of pages20
JournalmBio
Volume14
Issue number6
Early online date15 Nov 2023
DOIs
Publication statusPublished - 19 Dec 2023

Data Availability Statement

The data sets generated and/or analyzed during the current study are available from the corresponding author upon reasonable request. Supplemental files are available in the Dataverse repository at https://doi.org/10.7910/DVN/JPN2C4.

Acknowledgements

We acknowledge the support of the Bauer Core Facility at Harvard University for their help with sequencing. We also thank the Baliga lab for providing the ∆salactin strain. We also thank Patrick Stoddard and Elizabeth May for all the support with the biochemical experiments, as well as Paul Dieterle for the discussions on catastrophe models. We thank Simonetta Gribaldo and Nika Pende for their insightful comments on the manuscript. We thank the MBL Woods Hole Physiology course for providing a space for breakthroughs and discoveries in this project.

Funding

J.Z. was supported by a grant 203276 /l/16/Z from the Wellcome Trust and support from the NSF-Simons Center for Mathematical and Statistical Analysis of Biology at Harvard (award #1764269). A.S. acknowledges support from the NSF-MCB CAREER award (1651117). T.A.W. and E.R.R.M. acknowledge the support through the John Templeton Foundation (62220).

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