| Topic | Key points | Best supporting citations (with pqac ids) | Primary sources with year + URL |
|---|---|---|---|
| Identity/domains | Target verified as recA / PP_1629 / UniProt Q88ME4 from Pseudomonas putida KT2440, a canonical bacterial RecA-family recombinase. User-provided UniProt/domain context is consistent with conserved RecA architecture: AAA+ ATPase / P-loop NTPase core, RecA DNA recombination-repair domain, and RecA-like C-terminal region. P. putida carries a single canonical recA plus two lexA paralogs, with LexA1 acting as the main SOS partner of RecA. | (pqac-00000012, pqac-00000015, pqac-00000000) | Akkaya et al., 2021, Environmental Microbiology, https://doi.org/10.1111/1462-2920.15384; Abella et al., 2007, Journal of Bacteriology, https://doi.org/10.1128/JB.01213-07; Sabei et al., 2023, IJMS, https://doi.org/10.3390/ijms241914896 |
| Molecular function | Conserved RecA function is ATP-dependent homologous recombination: RecA nucleates on ssDNA, forms right-handed nucleoprotein filaments, conducts homology search, and catalyzes DNA strand exchange. ATP hydrolysis powers filament dynamics and strand exchange progression. Filaments assemble preferentially on ssDNA and may extend directionally. RecA also serves as the activated coprotease platform that enables LexA self-cleavage in SOS signaling. | (pqac-00000001, pqac-00000007, pqac-00000003, pqac-00000004) | Cox et al., 2023, MMBR, https://doi.org/10.1128/mmbr.00078-22; Carrasco et al., 2024, FEMS Microbiology Reviews, https://doi.org/10.1093/femsre/fuad065; Mudgal et al., 2024, PNAS Nexus, https://doi.org/10.1093/pnasnexus/pgae555; Bakhlanova et al., 2025 preprint, https://doi.org/10.1101/2024.05.07.592916 |
| SOS regulation in P. putida | In KT2440/EM173, activated RecA can fully cleave LexA1, but the overall SOS response is unusually weak relative to E. coli. Basal recA and lexA1 expression is high even without DNA damage, and inducibility by norfloxacin is only moderate. Cross-species complementation showed asymmetry: RecA_PP can efficiently support cleavage of LexA_EC, whereas RecA_EC poorly promotes cleavage of LexA1_PP. This supports the conclusion that KT2440 has limited SOS output because of inefficient RecA-LexA1 interplay plus promoter architecture and repression differences. | (pqac-00000008, pqac-00000009, pqac-00000010, pqac-00000011) | Akkaya et al., 2021, Environmental Microbiology, https://doi.org/10.1111/1462-2920.15384 |
| Organism-specific phenotypes/data | Under filament-inducing growth at 50 rpm, RecA or PP_1629 increased 2.35-fold. Filamented cultures showed 12.5-fold greater heat-shock resistance and 2.1-fold greater saline resistance than non-filamented cultures. RecA was required for the heat-shock resistance gain but not for filament formation itself. For formaldehyde, KT2440 tolerated up to 1.5 mM, while 10 mM was lethal, and 0.5 mM reduced growth rate by about 40 percent. recA mutants were hypersensitive at 10 mM formaldehyde, with killing 3 to 4 orders of magnitude higher or about 1000-fold faster than wild type. | (pqac-00000016, pqac-00000017, pqac-00000018, pqac-00000019, pqac-00000026) | Crabbé et al., 2012, BMC Microbiology, https://doi.org/10.1186/1471-2180-12-282; Roca et al., 2008, Microbial Biotechnology, https://doi.org/10.1111/j.1751-7915.2007.00014.x |
| Recent 2023-2024 developments | Recent work sharpened mechanistic understanding of RecA systems. A 2024 Pseudomonas aeruginosa cryo-EM and biophysical study resolved the activated RecA-LexA complex and quantified binding parameters: KDapp about 82 plus or minus 34 nM for RecA binding a 32-mer ssDNA, about 2.0 plus or minus 0.2 µM for ATPγS binding with ssDNA, and about 390 plus or minus 50 nM for LexA CTD binding to activated RecA. Broader 2023 to 2024 reviews emphasize RecA as the central bacterial recombinase for stalled-fork processing, postreplication-gap repair, and filament-based homology search and strand exchange. | (pqac-00000002, pqac-00000001, pqac-00000007, pqac-00000000) | Vascon et al., 2024 preprint, https://doi.org/10.1101/2024.03.22.585941; Cox et al., 2023, MMBR, https://doi.org/10.1128/mmbr.00078-22; Carrasco et al., 2024, FEMS Microbiology Reviews, https://doi.org/10.1093/femsre/fuad065; Sabei et al., 2023, IJMS, https://doi.org/10.3390/ijms241914896 |
| Applications | RecA-mediated homologous recombination remains a standard route for bacterial allelic exchange and suicide-plasmid knockouts, but it is often less efficient and more difficult operationally than phage recombineering systems such as lambda-Red or RecET. DNA uptake requirements and RecBCD-related constraints are practical limitations. For P. putida specifically, weak recombinogenic and SOS behavior helps explain why KT2440 can be harder to engineer by classical homologous recombination, even as this may contribute to genome stability. The 2024 Pseudomonas RecA-LexA structural study also provides a framework for SOS-targeting antimicrobial design. | (pqac-00000021, pqac-00000022, pqac-00000023, pqac-00000010, pqac-00000002) | Tong et al., 2023, PeerJ, https://doi.org/10.7717/peerj.15790; Li et al., 2023, Engineering Microbiology, https://doi.org/10.1016/j.engmic.2023.100097; Akkaya et al., 2021, Environmental Microbiology, https://doi.org/10.1111/1462-2920.15384; Vascon et al., 2024 preprint, https://doi.org/10.1101/2024.03.22.585941 |


*Table: This table summarizes the verified identity, core function, SOS biology, organism-specific phenotypes, recent mechanistic advances, and application relevance of RecA in Pseudomonas putida KT2440. It includes direct KT2440 evidence plus carefully labeled recent conserved RecA-family findings most relevant to functional annotation.*