Establishing genetic tractability in Jeongeupia sacculi HS-3: disruption of rpoS hinders biofilm formation
- 1Georgia Institute of Technology
Abstract
Jeongeupia sacculi (HS-3) is a novel {beta}-proteobacterium with a unique multicellular life cycle. The genetic tractability and mechanisms underlying differentiation are unknown. Here, we adapt a method of homologous recombination for genetic modification in HS-3 and generate a disruption mutant of rpoS, which encodes the alternative sigma factor{sigma} S commonly associated with general stress response or major behavioral switches. We then characterize phenotypes associated with rpoS disruption. Under low-nutrient conditions, rpoS disruption reduced Congo red binding, consistent with rpoS acting as a regulator of low-nutrient response by upregulating production of biofilm-associated materials. Surprisingly, rpoS disruption did not significantly alter survival in response to other stressors in general stress response assays tested. Our work establishes a method for genetic manipulation in HS-3 and enables future investigation into the life cycle of HS-3, including whether rpoS has a role in differentiation triggered by low-nutrient response.
Related
- Genetic disruption of cutaneous de novo glucocorticoid synthesis: a CRISPR-Cas9 CYP11B1-knockout human epidermal model
- Functional disruption of vgsc reveals haplosufficiency with implications for insecticide resistance and genetic control in Anopheles gambiae
- Acetaminophen-induced liver injury triggers short- and long-term neuroinflammation, blood-brain barrier disruption, and behavioral deficits in a genetic mouse model of autism.
- Genetic Disruption at the CIP2A Locus Modulates T Cell Responses and Attenuates Experimental Autoimmune Encephalomyelitis
- Genetic coupling of hydathode formation with leaf morphogenesis maintains water homeostasis
BibTeX
@misc{beddingfield2026establishing,
title = {{Establishing genetic tractability in Jeongeupia sacculi HS-3: disruption of rpoS hinders biofilm formation}},
author = {Z. Beddingfield and I. K. Calimlim and C. Zhang and B. K. Hammer},
howpublished = {bioRxiv},
year = {2026},
month = oct,
doi = {10.64898/2026.10.09.758012},
url = {https://www.biorxiv.org/content/10.64898/2026.10.09.758012v1},
note = {CC BY},
}
RIS
TY - UNPB
TI - Establishing genetic tractability in Jeongeupia sacculi HS-3: disruption of rpoS hinders biofilm formation
AU - Z. Beddingfield
AU - I. K. Calimlim
AU - C. Zhang
AU - B. K. Hammer
PY - 2026
DA - 2026/10/09
PB - bioRxiv
DO - 10.64898/2026.10.09.758012
UR - https://www.biorxiv.org/content/10.64898/2026.10.09.758012v1
AB - Jeongeupia sacculi (HS-3) is a novel {beta}-proteobacterium with a unique multicellular life cycle. The genetic tractability and mechanisms underlying differentiation are unknown. Here, we adapt a method of homologous recombination for genetic modification in HS-3 and generate a disruption mutant of rpoS, which encodes the alternative sigma factor{sigma} S commonly associated with general stress response or major behavioral switches. We then characterize phenotypes associated with rpoS disruption. Under low-nutrient conditions, rpoS disruption reduced Congo red binding, consistent with rpoS acting as a regulator of low-nutrient response by upregulating production of biofilm-associated materials. Surprisingly, rpoS disruption did not significantly alter survival in response to other stressors in general stress response assays tested. Our work establishes a method for genetic manipulation in HS-3 and enables future investigation into the life cycle of HS-3, including whether rpoS has a role in differentiation triggered by low-nutrient response.
ER -