PT  - JOURNAL ARTICLE
AU  - Alona Keren-Paz
AU  - Malena Cohen-Cymberknoh
AU  - Dror Kolodkin-Gal
AU  - Shani Peretz
AU  - Iris Karunker
AU  - Sharon G. Wolf
AU  - Tsviya Olender
AU  - Sergey Kapishnikov
AU  - Vlad Brumfield
AU  - Simon Dersch
AU  - Elena Kartvelishvily
AU  - Peninnah Green-Zelinger
AU  - Damilola Isola-Adeyanju
AU  - Ronit Suissa
AU  - Michal Shteinberg
AU  - Daniel McLeod
AU  - Marianna Patrauchan
AU  - Gideon Zamir
AU  - Assaf Gal
AU  - Peter L. Graumann
AU  - Eitan Kerem
AU  - Ilana Kolodkin-Gal
TI  - The formation of microbial exoskeletons is driven by a controlled calcium-concentrating subcellular niche
AID  - 10.1101/2020.01.08.898569
DP  - 2021 Jan 01
TA  - bioRxiv
PG  - 2020.01.08.898569
4099  - http://biorxiv.org/content/early/2021/05/25/2020.01.08.898569.short
4100  - http://biorxiv.org/content/early/2021/05/25/2020.01.08.898569.full
AB  - In nature, bacteria reside in biofilms - multicellular differentiated communities held together by extracellular matrix. In this work, we identified a novel subpopulation essential for biofilm formation – mineral-forming cells. This subpopulation contains an intracellular calcium-accumulating niche, in which the formation of a calcium carbonate mineral is initiated. As the biofilm colony develops, this mineral grows in a controlled manner, forming a functional macrostructure that serves the entire community.The molecular mechanisms promoting calcite scaffold formation were conserved between three distant phyla – the Gram-positive Bacillus subtilis, Gram-negative Pseudomonas aeruginosa and the actinobacterium Mycobacterium abscessus. Biofilm development of all three species was similarly impaired by inhibition of calcium uptake and carbonate accumulation. Moreover, chemical inhibition and mutations targeting mineralization both significantly reduced the attachment of P. aeruginosa to the lung, as well as the subsequent damage inflicted by biofilms to lung tissues, and restored their sensitivity to antibiotics.The evolutionary conserved cellular pathway controlling the fundamental feature of biofilm development uncovered in this work offers novel druggable targets for antibiotics to combat otherwise untreatable biofilm infections.Competing Interest StatementThe authors have declared no competing interest.