scholarly journals Signatures of host/symbiont genome coevolution in insect nutritional endosymbioses

2015 ◽  
Vol 112 (33) ◽  
pp. 10255-10261 ◽  
Author(s):  
Alex C. C. Wilson ◽  
Rebecca P. Duncan
Keyword(s):  
Amino Acid ◽  
Genome Evolution ◽  
Genetic Material ◽  
Cell Lineage ◽  
Host Cells ◽  
Cellular Mechanisms ◽  
New Era ◽  
Branched Chain ◽  
Symbiosis Research ◽  
Symbiont Genome

The role of symbiosis in bacterial symbiont genome evolution is well understood, yet the ways that symbiosis shapes host genomes or more particularly, host/symbiont genome coevolution in the holobiont is only now being revealed. Here, we identify three coevolutionary signatures that characterize holobiont genomes. The first signature, host/symbiont collaboration, arises when completion of essential pathways requires host/endosymbiont genome complementarity. Metabolic collaboration has evolved numerous times in the pathways of amino acid and vitamin biosynthesis. Here, we highlight collaboration in branched-chain amino acid and pantothenate (vitamin B5) biosynthesis. The second coevolutionary signature is acquisition, referring to the observation that holobiont genomes acquire novel genetic material through various means, including gene duplication, lateral gene transfer from bacteria that are not their current obligate symbionts, and full or partial endosymbiont replacement. The third signature, constraint, introduces the idea that holobiont genome evolution is constrained by the processes governing symbiont genome evolution. In addition, we propose that collaboration is constrained by the expression profile of the cell lineage from which endosymbiont-containing host cells, called bacteriocytes, are derived. In particular, we propose that such differences in bacteriocyte cell lineage may explain differences in patterns of host/endosymbiont metabolic collaboration between the sap-feeding suborders Sternorrhyncha and Auchenorrhynca. Finally, we review recent studies at the frontier of symbiosis research that are applying functional genomic approaches to characterization of the developmental and cellular mechanisms of host/endosymbiont integration, work that heralds a new era in symbiosis research.

Autophagy regulates whitefly–symbiont metabolic interactions

2021 ◽  
Author(s):  
Yan-Bin Wang ◽  
Ce Li ◽  
Jin-Yang Yan ◽  
Tian-Yu Wang ◽  
Ya-Lin Yao ◽  
...  
Keyword(s):  
Amino Acid ◽  
Essential Amino Acid ◽  
Critical Role ◽  
Dietary Supplementation ◽  
B Vitamins ◽  
Host Cells ◽  
Cellular Mechanisms ◽  
Essential Nutrients ◽  
Metabolic Interactions ◽  
B Vitamin

Nutritional symbionts are restricted to specialized host cells called bacteriocytes in various insect orders. These symbionts can provide essential nutrients to the host. However, the cellular mechanisms underlying the regulation of these insect–symbiont metabolic associations remain largely unclear. The whitefly, Bemisia tabaci MEAM1, hosts Portiera and Hamiltonella bacteria in the same bacteriocyte. In this study, the induction of autophagy by chemical treatment and gene silencing decreased symbiont titers, and essential amino acid (EAA) and B vitamin contents. In contrast, the repression of autophagy in bacteriocytes via Atg8 silencing increased symbiont titers, and amino acid and B vitamin contents. Furthermore, dietary supplementation with non-EAAs or B vitamins alleviated autophagy in whitefly bacteriocytes, elevated TOR (target of rapamycin) expression and increased symbiont titers. TOR silencing restored symbiont titers in whiteflies after dietary supplementation with B vitamins. These data suggest that Portiera and Hamiltonella evade autophagy of the whitefly bacteriocytes by activating the TOR pathway via providing essential nutrients. Taken together, we demonstrated that autophagy plays a critical role in regulating the metabolic interactions between the whitefly and two intracellular symbionts. Therefore, this study reveals that autophagy is an important cellular basis for bacteriocyte evolution and symbiosis persistence in whiteflies. The whitefly symbiosis unravels the interactions between cellular and metabolic functions of bacteriocytes. Importance Nutritional symbionts, which are restricted to specialized host cells called bacteriocytes, can provide essential nutrients for many hosts. However, the cellular mechanisms of regulation of animal–symbiont metabolic associations have been largely unexplored. Here, using the whitefly- Portiera / Hamiltonella endosymbiosis, we demonstrate autophagy regulates the symbiont titers, and thereby alters the essential amino acid and B vitamin contents. For persistence in the whitefly bacteriocytes, Portiera and Hamiltonella alleviate autophagy by activating the TOR (target of rapamycin) pathway through providing essential nutrients. Therefore, we demonstrate that autophagy plays a critical role in regulating the metabolic interactions between the whitefly and two intracellular symbionts. This study also provides insight into the cellular basis of bacteriocyte evolution and symbiosis persistence in the whitefly. The mechanisms underlying the role of autophagy in whitefly symbiosis could be widespread in many insect nutritional symbioses. These findings provide new avenue for whitefly control via regulating autophagy in the future.

scholarly journals Influence of excess branched-chain amino acid uptake by Streptococcus mutans in human host cells

2017 ◽  
Vol 365 (3) ◽  
Author(s):  
Takafumi Arimoto ◽  
Rei Yambe ◽  
Hirobumi Morisaki ◽  
Haruka Umezawa ◽  
Hideo Kataoka ◽  
...  
Keyword(s):  
Amino Acid ◽  
Streptococcus Mutans ◽  
Amino Acid Uptake ◽  
Host Cells ◽  
Acid Uptake ◽  
Human Host ◽  
Branched Chain Amino Acid ◽  
Branched Chain

scholarly journals Importance of Branched-Chain Amino Acid Utilization in Francisella Intracellular Adaptation

2014 ◽  
Vol 83 (1) ◽  
pp. 173-183 ◽  
Author(s):  
Gael Gesbert ◽  
Elodie Ramond ◽  
Fabiola Tros ◽  
Julien Dairou ◽  
Eric Frapy ◽  
...  
Keyword(s):  
Amino Acid ◽  
Critical Role ◽  
Cell Types ◽  
Host Cells ◽  
Metabolic Adaptation ◽  
Amino Acid Transporters ◽  
Loss Of Function ◽  
Content Type ◽  
Branched Chain Amino Acid ◽  
Branched Chain

Intracellular bacterial pathogens have adapted their metabolism to optimally utilize the nutrients available in infected host cells. We recently reported the identification of an asparagine transporter required specifically for cytosolic multiplication ofFrancisella. In the present work, we characterized a new member of the major super family (MSF) of transporters, involved in isoleucine uptake. We show that this transporter (here designated IleP) plays a critical role in intracellular metabolic adaptation ofFrancisella. Inactivation of IleP severely impaired intracellularF. tularensissubsp.novicidamultiplication in all cell types tested and reduced bacterial virulence in the mouse model. To further establish the importance of theilePgene inF. tularensispathogenesis, we constructed a chromosomal deletion mutant ofileP(ΔFTL_1803) in theF. tularensissubsp.holarcticalive vaccine strain (LVS). Inactivation of IleP in theF. tularensisLVS provoked comparable intracellular growth defects, confirming the critical role of this transporter in isoleucine uptake. The data presented establish, for the first time, the importance of isoleucine utilization for efficient phagosomal escape and cytosolic multiplication ofFrancisellaand suggest that virulentF. tularensissubspecies have lost their branched-chain amino acid biosynthetic pathways and rely exclusively on dedicated uptake systems. This loss of function is likely to reflect an evolution toward a predominantly intracellular life style of the pathogen. Amino acid transporters should be thus considered major players in the adaptation of intracellular pathogens.

scholarly journals Itaconate Alters Succinate and Coenzyme A Metabolism via Inhibition of Mitochondrial Complex II and Methylmalonyl-CoA Mutase

Metabolites ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 117
Author(s):  
Thekla Cordes ◽  
Christian M. Metallo
Keyword(s):  
Amino Acid ◽  
Metabolic Pathways ◽  
Mammalian Cells ◽  
Coenzyme A ◽  
Cultured Cells ◽  
Tca Cycle ◽  
Regulatory Function ◽  
Reversible Inhibitor ◽  
Complex Ii ◽  
Branched Chain

Itaconate is a small molecule metabolite that is endogenously produced by cis-aconitate decarboxylase-1 (ACOD1) in mammalian cells and influences numerous cellular processes. The metabolic consequences of itaconate in cells are diverse and contribute to its regulatory function. Here, we have applied isotope tracing and mass spectrometry approaches to explore how itaconate impacts various metabolic pathways in cultured cells. Itaconate is a competitive and reversible inhibitor of Complex II/succinate dehydrogenase (SDH) that alters tricarboxylic acid (TCA) cycle metabolism leading to succinate accumulation. Upon activation with coenzyme A (CoA), itaconyl-CoA inhibits adenosylcobalamin-mediated methylmalonyl-CoA (MUT) activity and, thus, indirectly impacts branched-chain amino acid (BCAA) metabolism and fatty acid diversity. Itaconate, therefore, alters the balance of CoA species in mitochondria through its impacts on TCA, amino acid, vitamin B12, and CoA metabolism. Our results highlight the diverse metabolic pathways regulated by itaconate and provide a roadmap to link these metabolites to potential downstream biological functions.

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