Research, Research Reports

Predictable regulation of survival by intratumoral microbe-immune crosstalk in patients with lung adenocarcinoma

Predictable regulation of survival by intratumoral microbe-immune crosstalk in patients with lung adenocarcinoma

Shuo Shi1, Yuwen Chu2,3, Haiyan Liu4,5, Lan Yu6,7,8, Dejun Sun8,9, Jialiang Yang2,3,5, Geng Tian2,3, Lei Ji2,3, Cong Zhang10 and Xinxin Lu11

Intratumoral microbiota can regulate the tumor immune microenvironment (TIME) and mediate tumor prognosis by promoting inflammatory response or inhibiting anti-tumor effects. Our study demonstrated that intratumoral microbiota-immune crosstalk was strongly associated with prognosis in LUAD patients, which would provide new targets for the development of precise therapeutic strategies.

Two TonB-dependent outer membrane transporters involved in heme uptake in <i>Anabaena</i> sp. PCC 7120

Two TonB-dependent outer membrane transporters involved in heme uptake in Anabaena sp. PCC 7120

Julia Graf1, Martin Schöpperle1,2, Rafael Pernil1 and Enrico Schleiff1,3,4

Low availability of micronutrients such as iron has enforced the evolution of uptake systems in all kingdoms of life. In our study, we conclude that heme transport might not be restricted to Anabaena, but at the same time is not specific to a cyanobacterial order and thus might be related to the habitat of origin, a notion which needs to be challenged in the future.

The last two transmembrane helices in the APC-type FurE transporter act as an intramolecular chaperone essential for concentrative ER-exit

The last two transmembrane helices in the APC-type FurE transporter act as an intramolecular chaperone essential for concentrative ER-exit

Yiannis Pyrris1, Georgia F. Papadaki1, Emmanuel Mikros2 and George Diallinas1,3

FurE is a H+ symporter specific for the cellular uptake of uric acid, allantoin, uracil, and toxic nucleobase analogues in the fungus Aspergillus nidulans. Being member of the NCS1 protein family, FurE is structurally related to the APC-superfamily of transporters.

Extracellular DNA secreted in yeast cultures is metabolism-specific and inhibits cell proliferation

Extracellular DNA secreted in yeast cultures is metabolism-specific and inhibits cell proliferation

Elisabetta de Alteriis1, Guido Incerti2, Fabrizio Cartenì3, Maria Luisa Chiusano3, Chiara Colantuono3, Emanuela Palomba4, Pasquale Termolino4, Francesco Monticolo3,5, Alfonso Esposito3, Giuliano Bonanomi3,6, Rosanna Capparelli3, Marco Iannaccone3,7, Alessandro Foscari2, Carmine Landi8, Palma Parascandola8, Massimo Sanchez9, Valentina Tirelli9, Bruna de Falco3, Virginia Lanzotti3 and Stefano Mazzoleni3,6

Our study demonstrates that extracellular DNA released by living cells can impact the growth rate of Saccharomyces cerevisiae cultures, showing similarities to extrachromosomal circular DNA and leading to cell cycle arrest in the S phase, suggesting potential new functional roles of exDNA.

Basal level of ppGpp coordinates <i>Escherichia coli</i> cell heterogeneity and ampicillin resistance and persistence

Basal level of ppGpp coordinates Escherichia coli cell heterogeneity and ampicillin resistance and persistence

Paulina Katarzyna Grucela1 and Yong Everett Zhang1

The universal stringent response alarmone ppGpp (guanosine penta and tetra phosphates) plays a crucial role in various aspects of fundamental cell physiology (e.g., cell growth rate, cell size) and thus bacterial tolerance to and survival of external stresses, including antibiotics. In tihs study, we discuss the fundamental role of basal level of ppGpp in regulating cell homogeneity and ampicillin persistence.

Investigation of the acetic acid stress response in <i>Saccharomyces cerevisiae</i> with mutated H3 residues

Investigation of the acetic acid stress response in Saccharomyces cerevisiae with mutated H3 residues

Nitu Saha1, Swati Swagatika1 and Raghuvir Singh Tomar1

Yeast cells respond to acetic acid in diverse ways. Here, we have elucidated the deleterious effects of acetic acid on different histone mutants

The coenzyme B<sub>12</sub> precursor 5,6-dimethylbenzimidazole is a flavin antagonist in <i>Salmonella</i>

The coenzyme B12 precursor 5,6-dimethylbenzimidazole is a flavin antagonist in Salmonella

Lahiru Malalasekara1 and Jorge C. Escalante-Semerena1,*

Here we investigated why 5,6-dimethylbenzimidazole (DMB) inhibits in S. Typhimurium. Briefly, we determined that the structural similarities of the substituted benzene ring of DMB with the isoalloxazine moiety of flavins is responsible for the deleterious effects of this CoB12 precursor.

Yeast gene <i>KTI13</i> (alias <i>DPH8</i>) operates in the initiation step of diphthamide synthesis on elongation factor 2

Yeast gene KTI13 (alias DPH8) operates in the initiation step of diphthamide synthesis on elongation factor 2

Meike Arend1, Koray Ütkür1, Harmen Hawer1, Klaus Mayer2, Namit Ranjan3, Lorenz Adrian4, Ulrich Brinkmann2 and Raffael Schaffrath1

We show here that apart from its effector role for Elongator-dependent tRNA modification in yeast, Kti13 alias Dph8 also operates in step one of the diphthamide modification pathway.

Caspase 3 exhibits a yeast metacaspase proteostasis function that protects mitochondria from toxic TDP43 aggregates

Caspase 3 exhibits a yeast metacaspase proteostasis function that protects mitochondria from toxic TDP43 aggregates

Steve Brunette1,#, Anupam Sharma1,2,#, Ryan Bell1, Lawrence Puente1 and Lynn A Megeney1,2,3,*

Caspase 3 activation is a hallmark of cell death and there is a strong correlation between elevated protease activity and evolving pathology in neurodegenerative disease, such as amyotrophic lateral sclerosis (ALS). These results suggest that caspase 3 is not inherently pathogenic, but may act as a compensatory proteostasis factor, to limit TDP-43 protein inclusions and protect organelle function in aggregation related degenerative disease.

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Early manifestations of replicative aging in the yeast Saccharomyces cerevisiae.

January 4, 2014

The data preseted herein suggest that retrograde signaling starts to malfunction in relatively young cells, leading to accumulation of heterogeneous mitochondria within one cell. The latter may further contribute to a decline in stress resistances.

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