The emergence of multidrug resistance (MDR) has become
a global health threat due to the increasing unnecessary use
of antibiotics. Multidrug resistant bacteria occur mainly by
accumulating resistance genes on mobile genetic elements
(MGEs), made possible by horizontal gene transfer (HGT).
Humans and animal guts along with natural and engineered
environments such as wastewater treatment plants and manured
soils have proven to be the major reservoirs and hotspots
of spreading antibiotic resistance genes (ARGs). As those
environments support the dissemination of MGEs through
the complex interactions that take place at the human-animalenvironment
interfaces, a growing One Health challenge is
for multiple sectors to communicate and work together to
prevent the emergence and spread of MDR bacteria. However,
maintenance of ARGs in a bacterial chromosome and/or
plasmids in the environments might place energy burdens
on bacterial fitness in the absence of antibiotics, and those
unnecessary ARGs could eventually be lost. This review highlights
and summarizes the current investigations into the gain
and loss of ARG genes in MDR bacteria among human-animal-
environment interfaces. We also suggest alternative treatments
such as combinatory therapies or sequential use of different
classes of antibiotics/adjuvants, treatment with enzymeinhibitors,
and phage therapy with antibiotics to solve the
MDR problem from the perspective of One Health issues.
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A novel bacterium, designated strain RR4-56T, was isolated
from a biofilter of a seawater recirculating aquaculture system.
The 16S rRNA gene sequence analysis showed that the
isolate was closely related to Halovulum dunhuangense YYQ-
30T (92.6%), Albimonas donghaensis DS2T (91.3%), Pontivivens
insulae GYSW-23T (91.3%), and Monaibacterium marinum
C7T (90.9%), belonging to the family Rhodobacteraceae.
The strain was aerobic, Gram-negative, rod-shaped, oxidasepositive,
and catalase-negative. Its optimum temperature,
pH, and salinity for growth were 25–30°C, pH 8.5, and 2–3%
NaCl (w/v), respectively. Its growth occurred at 15–35°C, pH
5.0–9.5, and 0–7% NaCl (w/v). It contained ubiquinone-10
(Q-10), a respiratory quinone, and the major cellular fatty
acids were 11-methyl C18:1 ω7c (31.9%), C18:1 ω6c (30.4%),
and C19:0 cyclo ω8c (16.1%). The polar lipids present in the
strain were phosphatidylglycerol, an unidentified phospholipid,
and an unidentified aminolipid. The strain had one
4,373,045 bp circular chromosome with G + C contents of
65.9 mol% including 4,169 genes, 4,118 coding sequences
(CDSs), 3 rRNAs, and 45 tRNAs. Genome annotation predicted
some gene clusters related to the degradation of several
types of organic matter such as protocatechuate, catechol,
and phthalate. Based on the polyphasic characteristics,
RR4-56T represents a novel genus and species in the family
Rhodobacteraceae, for which the name Pikeienuella piscinae
gen. nov., sp. nov. was proposed. The type strain is RR4-56T
(= KCTC 52648T = DSM 107918T).
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and phosphatidylinositol, and those of strains
HDW15BT and HDW15CT were sphingoglycolipid, diphosphatidylglycerol,
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and phosphatidylcholine. The G + C content of strains
HDW12AT, HDW15BT, and HDW15CT were 69.7, 63.3, and
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the names Nocardioides piscis for strain HDW12AT (= KACC
21336T = KCTC 49321T = JCM 33670T), Sphingomonas piscis
for strain HDW15BT (= KACC 21341T = KCTC 72588T = JCM
33738T), and Sphingomonas sinipercae for strain HDW15CT
(= KACC 21342T = KCTC 72589T = JCM 33739T).
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The SbcCD complex is an essential component of the DNA
double-strand break (DSB) repair system in bacteria. The
bacterial SbcCD complex recognizes and cleaves the DNA
ends in DSBs by ATP-dependent endo- and exonuclease
activities as an early step of the DNA repair process. SbcD
consists of nuclease, capping, and helix-loop-helix domains.
Here, we present the crystal structure of a SbcD fragment from
Staphylococcus aureus, which contained nuclease and capping
domains, at a resolution of 2.9 Å. This structure shows
a dimeric assembly similar to that of the corresponding domains
of SbcD from Escherichia coli. The S. aureus SbcD fragment
exhibited endonuclease activities on supercoiled DNA
and exonuclease activity on linear and nicked DNA. This
study contributes to the understanding of the molecular basis
for how bacteria can resist sterilizing treatment, causing DNA
damage.
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Staphylococcus aureus SOS response: Activation, impact, and drug targets Kaiying Cheng, Yukang Sun, Huan Yu, Yingxuan Hu, Yini He, Yuanyuan Shen mLife.2024; 3(3): 343. CrossRef
Although colistin is frequently regarded as the antibiotic of
last resort in treating carbapenem-resistant Klebsiella pneumoniae,
colistin heteroresistance may in part be associated
with antibiotic treatment failure. However, we do not know
how widespread the colistin heteroresistance is in carbapenem-
resistant K. pneumoniae isolates. In this study, we performed
colistin disc diffusion assays, E-tests, and population
analysis profiling for KPC-2-producing K. pneumoniae isolates
to identify colistin heteroresistance. Although no colistin-
resistant colonies were detected by the disc diffusion
test and E-test, a colistin-resistant subpopulation was identified
in population analysis profiling in all colistin-susceptible,
KPC-2-producing K. pneumoniae isolates. Colistin-resistant
subpopulations were also identified even when isolates
had no colistin exposure. The ratio of colistin-resistant
subpopulations to the total population increased as the exposure
concentration of colistin increased. In in vitro time-kill
assays, regrowth was observed in all isolates after 2 h upon
exposure to colistin. We identified common amino acid alterations
in PhoQ, PhoP, and PmrB in colistin-resistant subpopulations
from some isolates, but no substitutions were
found in most resistant subpopulations from other isolates.
In all colistin-resistant subpopulations, overexpression of
PhoQ and PbgP was observed. In this study, we demonstrated
that colistin heteroresistance may be common in KPC-2-producing
K. pneumoniae isolates, which could not be detected
in the disc diffusion method and E-test. Colistin heteroresistance
may cause colistin treatment failure in part and may
evolve into resistance. Thus, development of more reliable
diagnostic methods is required to detect colistin heteroresistance.
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Aroma ester components produced by fermenting yeast cells
via alcohol acetyltransferase (AATase)-catalyzed intracellular
reactions are responsible for the fruity character of fermented
alcoholic beverages, such as beer and wine. Acetate esters
are reportedly produced at relatively high concentrations by
non-Saccharomyces species. Here, we identified 12 ATF orthologues
(SfATFs) encoding putative AATases, in the diploid
genome of Saccharomycopsis fibuligera KJJ81, an isolate from
wheat-based Nuruk in Korea. The identified SfATF proteins
(SfAtfp) display low sequence identities with S. cerevisiae
Atf1p (between 13.3 and 27.0%). All SfAtfp identified, except
SfAtf(A)4p and SfAtf(B)4p, contained the activation domain
(HXXXD) conserved in other Atf proteins. Culture supernatant
analysis using headspace gas chromatography mass spectrometry
confirmed that the recombinant S. cerevisiae strains
expressing SfAtf(A)2p, SfAtf(B)2p, and SfAtf(B)6p produced
high levels of isoamyl and phenethyl acetates. The volatile
aroma profiles generated by the SfAtf proteins were distinctive
from that of S. cerevisiae Atf1p, implying difference in
the substrate preference. Cellular localization analysis using
GFP fusion revealed the localization of SfAtf proteins proximal
to the lipid particles, consistent with the presence of amphipathic
helices at their N- and C-termini. This is the first
report that systematically characterizes the S. fibuligera ATF
genes encoding functional AATases responsible for acetate
ester formation using higher alcohols as substrate, demonstrating
their biotechnological potential for volatile ester production.
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Phylogenomic tree reconstruction has recently become a
routine and critical task to elucidate the evolutionary relationships
among bacterial species. The most widely used method
utilizes the concatenated core genes, universally present in a
single-copy throughout the bacterial domain. In our previous
study, a bioinformatics pipeline termed Up-to-date Bacterial
Core Genes (UBCG) was developed with a set of bacterial core
genes selected from 1,429 species covering 28 phyla. In this
study, we revised a new bacterial core gene set, named UBCG2,
that was selected from the more extensive genome sequence
set belonging to 3,508 species spanning 43 phyla. UBCG2 comprises
81 genes with nine Clusters of Orthologous Groups of
proteins (COGs) functional categories. The new gene set and
complete pipeline are available at http://leb.snu.ac.kr/ubcg2.
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Human papillomaviruses (HPVs) are known to utilize the
down-regulation of epithelial (E)-cadherin, a major component
of adherens junctions of keratinocytes, to evade host
immune surveillance in high-risk group. However, the effects
of HPV on the function of E-cadherin in low-risk groups remain
unknown. We investigated whether type 2 HPV (HPV-
2) E7 could induce alterations in E-cadherin expression in
transiently transfected keratinocytes and cell lines expressing
HPV-2 E7. To examine the expression pattern of E-cadherin
in cutaneous warts and normal skin samples, immunohistochemical
analysis was performed. Quantitative real-time
polymerase chain reactions, luciferase assays, western blot,
immunocytochemistry, and electron microscopy were used
to evaluate the mRNA and protein expression levels of Ecadherin
in normal human epidermal keratinocytes transfected
with HPV-2 E7 plasmid DNA or E7-specific siRNA
and in E7-expressing cell lines. E-cadherin expression levels
in HPV-2 positive cutaneous warts were significantly decreased
compared to those in normal skin (p < 0.05). Similarly,
the mRNA and protein expression levels of E-cadherin
in E7 transiently transfected cells were significantly decreased
compared to those in empty vector-transfected cells. The decreases
were restored by transfection with E7-specific siRNA
(p < 0.05). Likewise, cell lines expressing E7 showed a decreased
expression of E-cadherin. When the cells were cultured
in low attachment plates, cell-to-cell aggregation was
inhibited. Taken together, our data suggest that HPV-2 E7,
the causative agent of cutaneous warts, could mediate the
transcriptional repression of E-cadherin.
Citations
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