Bacteria employ a diverse array of cellular regulatory
mechanisms to successfully adapt and thrive in ever-changing
environments, including but not limited to temperature
changes, fluctuations in nutrient availability, the presence
or absence of electron acceptors such as oxygen, the availability
of metal ions crucial for enzyme activity, and the
existence of antibiotics. Bacteria can virtually modulate
any step of gene expression from transcr!ptional initiation
to posttranslational modification of a protein for the control
of cellular processes. Furthermore, one gene regulator
often controls another in a complex gene regulatory network.
Thus, it is not easy to fully understand the intricacies of
bacterial regulatory mechanisms in various environments. In
this special issue, while acknowledging the challenge of covering
all aspects of bacterial regulatory mechanisms across
diverse environments, seven review articles are included to
provide insight into the recent progress in understanding
such mechanisms from different perspectives: positive regulatory
mechanisms by secondary messenger (cAMP receptor
protein), two-component signal transduction mechanisms
(Rcs and Cpx), diverse regulatory mechanisms by a specific
environmental factor in specific bacteria (oxygen availability
in Mycobacterium and manganese ion availability in Salmonella),
diverse regulatory mechanisms by a specific environmental
factor (temperature and antibiotics), and regulatory
mechanisms by antibiotics in cell wall synthesis.
Bacteria, as ubiquitous organisms that can be found in
almost every environment, carry out complex cellular processes
that allow them to survive and thrive in a variety of
different conditions despite their small size and relative simplicity.
One of the key factors that allows bacteria to carry
out these complex processes is their ability to regulate gene
expression through various mechanisms. Gene expression
is a fundamental biological process by which the genetic
information encoded in a gene is transcribed into an RNA
molecule and subsequently translated into a functional gene
product, often a protein. Furthermore, the activity levels of
proteins may further be altered by posttranslational modification.
Regulation of gene expression refers to the control
of the amount and timing of gene expression, and thus it
can be divided into transcr!ptional, translational, and posttranslational
levels.
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The PhoBR two-component system upregulates virulence in Aeromonas dhakensis C4–1 Wei Feng, Xuesong Li, Nuo Yang, Lixia Fan, Guiying Guo, Jun Xie, Xiuqing Cai, Yuqi Meng, Jifeng Zeng, Yu Han, Jiping Zheng Aquaculture.2025; 595: 741665. CrossRef
Molecular mechanisms of cold stress response in cotton: Transcriptional reprogramming and genetic strategies for tolerance Washu Dev, Fahmida Sultana, Hongge Li, Daowu Hu, Zhen Peng, Shoupu He, Haobo Zhang, Muhammad Waqas, Xiaoli Geng, Xiongming Du Plant Science.2025; 352: 112390. CrossRef
PhoPQ-mediated lipopolysaccharide modification governs intrinsic resistance to tetracycline and glycylcycline antibiotics in
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The active and inactive structures of the Escherichia coli cAMP receptor protein (CRP), a model bacterial transcr!ption
factor, are compared to generate a paradigm in the cAMP-induced activation of CRP. The resulting paradigm is shown to be
consistent with numerous biochemical studies of CRP and CRP*, a group of CRP mutants displaying cAMP-free activity.
The cAMP affinity of CRP is dictated by two factors: (i) the effectiveness of the cAMP pocket and (ii) the protein equilibrium
of apo-CRP. How these two factors interplay in determining the cAMP affinity and cAMP specificity of CRP and CRP*
mutants are discussed. Both the current understanding and knowledge gaps of CRP-DNA interactions are also described.
This review ends with a list of several important CRP issues that need to be addressed in the future.
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cAMP-independent DNA binding of the CRP family protein DdrI from
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The metal cofactors are essential for the function of many enzymes. The host restricts the metal acquisition of pathogens for
their immunity and the pathogens have evolved many ways to obtain metal ions for their survival and growth. Salmonella
enterica serovar Typhimurium also needs several metal cofactors for its survival, and manganese has been found to contribute
to Salmonella pathogenesis. Manganese helps Salmonella withstand oxidative and nitrosative stresses. In addition,
manganese affects glycolysis and the reductive TCA, which leads to the inhibition of energetic and biosynthetic metabolism.
Therefore, manganese homeostasis is crucial for full virulence of Salmonella. Here, we summarize the current information
about three importers and two exporters of manganese that have been identified in Salmonella. MntH, SitABCD, and ZupT
have been shown to participate in manganese uptake. mntH and sitABCD are upregulated by low manganese concentration,
oxidative stress, and host NRAMP1 level. mntH also contains a Mn2+-
dependent riboswitch in its 5′ UTR. Regulation of
zupT expression requires further investigation. MntP and YiiP have been identified as manganese efflux proteins. mntP is
transcr!ptionally activated by MntR at high manganese levels and repressed its activity by MntS at low manganese levels.
Regulation of yiiP requires further analysis, but it has been shown that yiiP expression is not dependent on MntS. Besides
these five transporters, there might be additional transporters that need to be identified.
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Mycobacterium tuberculosis is the causative agent of tuberculosis. M. tuberculosis can survive in a dormant state within
the granuloma, avoiding the host-mounting immune attack. M. tuberculosis bacilli in this state show increased tolerance
to antibiotics and stress conditions, and thus the transition of M. tuberculosis to the nonreplicating dormant state acts as
an obstacle to tuberculosis treatment. M. tuberculosis in the granuloma encounters hostile environments such as hypoxia,
nitric oxide, reactive oxygen species, low pH, and nutrient deprivation, etc., which are expected to inhibit respiration of M.
tuberculosis. To adapt to and survive in respiration-inhibitory conditions, it is required for M. tuberculosis to reprogram its
metabolism and physiology. In order to get clues to the mechanism underlying the entry of M. tuberculosis to the dormant
state, it is important to understand the mycobacterial regulatory systems that are involved in the regulation of gene expression
in response to respiration inhibition. In this review, we briefly summarize the information regarding the regulatory
systems implicated in upregulation of gene expression in mycobacteria exposed to respiration-inhibitory conditions. The
regulatory systems covered in this review encompass the DosSR (DevSR) two-component system, SigF partner switching
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The global public health burden of bacterial antimicrobial resistance (AMR) is intensified by Gram-negative bacteria,
which have an additional membrane, the outer membrane (OM), outside of the peptidoglycan (PG) cell wall. Bacterial twocomponent
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results in NlpE retention in the inner membrane, provoking the Cpx response. Signaling requires the NlpE NTD, but
not the NlpE CTD; however, OM-anchored NlpE senses adherence to a hydrophobic surface, with the NlpE CTD playing
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Bacterial cells are covered with various glycopolymers such as peptidoglycan (PG), lipopolysaccharides (LPS), teichoic
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