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Interactions Between Virocells and Their Environment Shape Macromolecules, Bacterial Populations, and Resource Partitioning /

Record Type:	Electronic resources : Monograph/item
Title/Author:	Interactions Between Virocells and Their Environment Shape Macromolecules, Bacterial Populations, and Resource Partitioning // Morgan Marie Lindback.
Author:	Lindback, Morgan Marie,
Description:	1 electronic resource (170 pages)
Notes:	Source: Dissertations Abstracts International, Volume: 86-03, Section: B.
Contained By:	Dissertations Abstracts International86-03B.
Subject:	Microbiology. -
Online resource:	https://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=31631092
ISBN:	9798384042310

Interactions Between Virocells and Their Environment Shape Macromolecules, Bacterial Populations, and Resource Partitioning /
Lindback, Morgan Marie,

Interactions Between Virocells and Their Environment Shape Macromolecules, Bacterial Populations, and Resource Partitioning /Morgan Marie Lindback. - 1 electronic resource (170 pages)

Source: Dissertations Abstracts International, Volume: 86-03, Section: B.

Viruses are the most abundant biological entity in the oceans, yet their impact on microbial populations and biogeochemical cycles remains poorly understood. This dissertation examines viral infections of bacteria in oceans by evaluating infections across environments and characterizing their resource use. Here, I combine laboratory experiments and computational approaches to understand the impact of viral infections across macromolecules, host populations, and gene evolution through the lens of environmental nutrients.First, I characterize metabolic reprogramming of two different viral infections of the same host in a low-phosphorus (P) environment using multi-omics (transcriptomics, proteomics, lipidomics, and endo- and exo-metabolomics). I found that low-P imposed common cellular responses on all cells (infected and uninfected cells), including a P-stress response, decreased transcription and translation, and less organic matter consumption. Low-P also imposed infection-specific responses (both infections), including enhancing nitrogen assimilation and fatty acid degradation, and decreasing extracellular lipid relative abundance. Virocell-specific strategies (differences between viruses) such as regulation of gene expression and retaining host proteins were also observed, which pointed to the phages' different needs for resource acquisition. Overall, this work contributes to our understanding of the breadth of metabolic reprogramming and environmental consequences of viral infection between different viruses and different environmental conditions.Second, I directly measure the impact of viral infection on carbon (C) and nitrogen (N) uptake by heterotrophic bacteria, track their population dynamics, and quantify changes in dissolved organic matter (DOM). I made three isotopically-labeled DOM environments that differed in their origins (phytoplankton and infected bacteria vs phytoplankton and uninfected bacteria vs phytoplankton) and then determined 13C and 15N incorporation of infected and uninfected heterotrophic bacteria in those three DOM-types using nanoSIMS. I found that the highest bacterial populations occurred in DOM made by other bacteria, regardless of infection, which suggests that bacteria feed bacteria. I next asked how bacterial biomass derived from DOM (Cnet and Nnet) changed with infection. I found that relative 13C and 15N incorporation between infected and uninfected bacteria is not the same across DOM sources, showing that resource use by infected heterotrophic bacteria differs with environment. This work shows that who makes DOM alters DOM composition, nutrient uptake, and microbial populations.Third, I determine evolutionary patterns of viral gene fitness within and between microscale environments (particle-associated, free-living, viral- fractions) using a metagenomic dataset from the global oceans. I used single codon variants of viral genes and their nonsynonymous to synonymous (pN/pS) ratios to determine evolutionary forces and resource costs of genomic variation. I found that viral gene functions were partitioned across microscales such that very few functions were found across all. Additionally, most (>96%) viral genes exhibited negative selection. Of all three fractions, the particle-associated fraction had the highest proportion of viral genes under positive selection, which metadata suggests may be a result of increased microbial interactions on particles. Finally, I show that the most frequently used codons have lower C and N content than variants, suggesting resource-driven selection within viral genes at the codon-level.This body of work illustrates how the environment shapes viral infection of bacteria, how infections alters the environment, and the evolutionary consequences of the interactions between infected cells and their environment.

English

ISBN: 9798384042310Subjects--Topical Terms:

536250
Microbiology.
Subjects--Index Terms:

Microbial ecology

Interactions Between Virocells and Their Environment Shape Macromolecules, Bacterial Populations, and Resource Partitioning /
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520 $a Viruses are the most abundant biological entity in the oceans, yet their impact on microbial populations and biogeochemical cycles remains poorly understood. This dissertation examines viral infections of bacteria in oceans by evaluating infections across environments and characterizing their resource use. Here, I combine laboratory experiments and computational approaches to understand the impact of viral infections across macromolecules, host populations, and gene evolution through the lens of environmental nutrients.First, I characterize metabolic reprogramming of two different viral infections of the same host in a low-phosphorus (P) environment using multi-omics (transcriptomics, proteomics, lipidomics, and endo- and exo-metabolomics). I found that low-P imposed common cellular responses on all cells (infected and uninfected cells), including a P-stress response, decreased transcription and translation, and less organic matter consumption. Low-P also imposed infection-specific responses (both infections), including enhancing nitrogen assimilation and fatty acid degradation, and decreasing extracellular lipid relative abundance. Virocell-specific strategies (differences between viruses) such as regulation of gene expression and retaining host proteins were also observed, which pointed to the phages' different needs for resource acquisition. Overall, this work contributes to our understanding of the breadth of metabolic reprogramming and environmental consequences of viral infection between different viruses and different environmental conditions.Second, I directly measure the impact of viral infection on carbon (C) and nitrogen (N) uptake by heterotrophic bacteria, track their population dynamics, and quantify changes in dissolved organic matter (DOM). I made three isotopically-labeled DOM environments that differed in their origins (phytoplankton and infected bacteria vs phytoplankton and uninfected bacteria vs phytoplankton) and then determined 13C and 15N incorporation of infected and uninfected heterotrophic bacteria in those three DOM-types using nanoSIMS. I found that the highest bacterial populations occurred in DOM made by other bacteria, regardless of infection, which suggests that bacteria feed bacteria. I next asked how bacterial biomass derived from DOM (Cnet and Nnet) changed with infection. I found that relative 13C and 15N incorporation between infected and uninfected bacteria is not the same across DOM sources, showing that resource use by infected heterotrophic bacteria differs with environment. This work shows that who makes DOM alters DOM composition, nutrient uptake, and microbial populations.Third, I determine evolutionary patterns of viral gene fitness within and between microscale environments (particle-associated, free-living, viral- fractions) using a metagenomic dataset from the global oceans. I used single codon variants of viral genes and their nonsynonymous to synonymous (pN/pS) ratios to determine evolutionary forces and resource costs of genomic variation. I found that viral gene functions were partitioned across microscales such that very few functions were found across all. Additionally, most (>96%) viral genes exhibited negative selection. Of all three fractions, the particle-associated fraction had the highest proportion of viral genes under positive selection, which metadata suggests may be a result of increased microbial interactions on particles. Finally, I show that the most frequently used codons have lower C and N content than variants, suggesting resource-driven selection within viral genes at the codon-level.This body of work illustrates how the environment shapes viral infection of bacteria, how infections alters the environment, and the evolutionary consequences of the interactions between infected cells and their environment.
546 $a English
590 $a School code: 0127
650 4 $a Microbiology. $3 536250
650 4 $a Ecology. $3 516476
650 4 $a Biological oceanography. $3 2122748
650 4 $a Biogeochemistry. $3 545717
650 4 $a Virology. $3 642304
653 $a Microbial ecology
653 $a Oceans
653 $a Viruses
653 $a Virocells
653 $a Bacterial populations
653 $a Macromolecules
690 $a 0329
690 $a 0410
690 $a 0416
690 $a 0720
690 $a 0425
710 2 $a University of Michigan. $b Ecology and Evolutionary Biology. $e degree granting institution. $3 3816898
720 1 $a Duhaime, Melissa B. $e degree supervisor.
773 0 $t Dissertations Abstracts International $g 86-03B.
790 $a 0127
791 $a Ph.D.
792 $a 2024
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