Genetic traits such as dominant or recessive phenotype of an identified cellular protein could be tested directly through haploid or diploid stages of the yeast life cycle. Finally, an identified cellular factor could also be verified by functional complementation using yeast or other eukaryotic homologues in respective cells. In fact, many human proteins that are important to human biology or diseases such as cancer-associated proteins were first discovered by studying their homologs in yeasts.
For reviews of related topics, see 8 , 9 , 10 , There are also many benefits of using yeasts as model systems to study viruses of higher eukaryotes such as plant, animal or human viruses.
The main reason is because yeasts carry their own indigenous viruses. For example, studies of yeast killer viruses have helped us to study cellular necrosis and apoptosis during virus-host interaction 14 , 15 , 16 , 17 , and to understand potential cellular viral restriction factors toward viral infections 18 , Since the integration process of yeast retrotransposons resembles in many ways retroviral integration, molecular studies of fission yeast Tf elements or budding yeast Ty elements provided insights into functions of retroviruses such as HIV or murine leukemia viruses 20 , 21 , For example, the first report showing yeast as a host for the replication of a plant viral genome was from Brome mosaic virus BMV , which is a member of the alphavirus-like superfamily of animal and plant positive strand RNA viruses Price et al.
Besides the RNA viruses, the genomes of multiple human papillomavirus HPV subtypes and bovine papillomavirus BPV type 1 can stably replicate in yeast in an E1 or E2-independent manner as nuclear plasmids 25 , This HPV viral gene E1 is a helicase, and E2 is a transcriptional activator and plasmid maintenance factor.
Both are known to contribute to the episomal replication of the viral genome Note: Modified and updated based on Note that ASBVd is a viroid not a virus per se.
Yeasts also have much smaller genomes than higher eukaryotes. Study of higher eukaryotic viruses that replicate in yeasts could aid study of core relationship between a viral function and cellular proteins, thus avoiding high complexity and redundancy of higher eukaryotic systems.
Cellular factors that are involved in viral DNA replication can thus be identified by exposing the viral replication apparatus to those genomic libraries. In this case, loss or reduction of the viral replication in the absence of a cellular protein would suggest requirement or involvement of this cellular protein in viral replication. Similarly, cellular viral restriction factors could potentially be uncovered by overproduction of a genomic or cDNA plasmid library in the viral replicating yeast cells.
Finally, many of the experimental approaches used in yeasts are not readily achievable in mammalian cells. For example, multiple and permanent heterologous gene-producing yeast strains can be established and maintained in the laboratory that allow simultaneous and batch testing repeatedly, thus facilitating large-scale and functional characterization of genes of interest such as a small viral genome 35 , Therefore, study of virus-cell interaction by taking advantage of the simplicity, biosafety and genetic amenability of yeasts can often reveal novel scientific findings that are not always easy to discover solely by relying on high eukaryotic systems.
Budding yeast S. It has about 5, protein-coding genes, with about 4. The daughter cells that are generated during cell division are generally smaller than mother cells Fig.
The optimum temperature for growth of S. Standard synthetic defined SD minimal medium is used to grow auxotrophic yeast cultures or select for yeast transformants containing plasmids. The selection media are generated by adding defined mixture of amino acids, vitamins and other components known as the drop-out supplements. Antibiotics such as hygromycin B and kanamycin can also be used as selectable markers 39 , Diagrams show yeasts have both asexual vegetative and sexual reproductive cycles, respectively.
A Budding yeast is generally maintained in the laboratory through vegetative growth both as haplontic haploid and diplontic diploid cells during asexual life cycle by mitosis, which produce daughter cells by budding off of mother cells.
Mitotic cell cycle has all of the typical eukaryotic cell cycle stages of G1, S, G2 and M phases, but it spends most of its cell cycling in G1 phase, which is similar to human cell cycle. Under stressful conditions, diploid cells undergo meiosis to form haploid spores by sporulation. B Fission yeast is normally present as haploid cells through mitosis.
Cells are divided equally between daughter and mother cells. In contrast to budding yeast cell cycle, fission yeast spends most of its cell cycling in G2 phase. Like other fungi, the life cycle of both budding and fission yeasts undergo asexual and sexual reproductive cycles Fig.
They are generally maintained in the laboratory through vegetative growth by asexual reproduction Unlike fission yeast, budding yeast reproduces both as haplontic haploid and diplontic diploid cells during asexual life cycle by mitosis Fig. However, under high-stress conditions such as nutrient starvation, haploid cells will die; while diploid cells undergo meiosis to form haploid spores by sporulation 42 , Budding yeast grows and divides through an asymmetric budding process.
During mitosis, the daughter cell begins to form as a small bud on the tip of the mother cell. At metaphase, one set of sister chromatids moves into the bud. Continued growth of the bud eventually becomes a separated daughter cell. Budding yeasts have all of the typical eukaryotic cell cycle stages of G1, S, G2 and M mitosis phases, which can be recognized by DNA content, nuclear morphology and bud morphology. Budding yeast spends most of its cell cycling in G1 phase, which is similar to human cell cycle.
Nearly all of the major cell cycle regulators identified in budding yeast have their counterparts in mammalian cells 4. Budding yeast has been used extensively as a model to study virus-host interactions and cellular restriction factors to viral infections 45 , Genome-wide approaches have been used in budding yeast to study various virus-related activities including viral transcription, viral replication and virus-host interactions 46 , 47 , 48 , 49 , General reviews on these topics are available 27 , 45 , 46 , 51 , Fission yeast S.
Its genome has approximately 1. It is estimated to have about 5, protein-coding genes. Subcellular locations of almost all fission yeast proteins are known The optimal growth temperature for S. The most commonly used growth medium with all of the necessary nutrients is the Standard Yeast Extract with Supplements YES medium, which is normally used to grow fission yeast cells without selection.
In order to select for a LEU2 or URA4 -carrying plasmid, the EMM medium needs to be supplemented with leucine or uracil to complement the corresponding auxotrophic mutants of a yeast strain. Antibiotics such as cycloheximide and Zeocin have also been used to select for hygromycin and bleMX6 resistance in fission yeast cells 56 , Fission yeast is normally present as haplontic cells but its diploid form could be triggered during meiosis by mating when cells were subject to nutritional starvation Fig.
Fusion of the two cells results in the formation of diploid zygotes. Sporulation is followed immediately by meiosis to produce four round or oval haploid ascospores that are enclosed within an ascus. When appropriate nutrients are resumed to allow cells re-entering its asexual life cycle, the ascus wall will disintegrate, and ascospores will germinate and eventually divide to form haploid clones 8 , The fission yeast cell maintains its shape by growing exclusively through its cell tips.
After mitosis, cell division occurs by medial fission with the formation of a septum that cleaves the cell at its midpoint to produce two equal sized cells Fig. Its specific length corresponds well with its growth phase in the cell cycle 61 , 62 , which is similar to that of other eukaryotes, and includes the G1, S, G2, and M phases.
However, S. In addition, the fission yeast nuclear envelope remains intact throughout mitosis. Therefore, all transactions involving the chromosomes during this phase occur within the nucleus. Fission yeast has been used extensively to study cell cycle regulation, DNA damage and repair as well as DNA replication.
For example, like budding yeast, nearly all of the major cell cycle regulators identified in fission yeast have their counterparts in mammalian cells 4 , 5. It has also been used as a host system to study virus-host interactions including the effect of viral proteins on cell cycle regulation 63 , 64 , gene expression, cell death and apoptosis 65 , 66 , In addition, fission yeast has been used to carry out large-scale and functional characterization of small viral genomes such as human immunodeficiency virus type 1 HIV-1 and Zika virus ZIKV 55 , 68 , 69 , General reviews on some of the related topics have been published previously 11 , 22 , 64 , 71 , 72 , 73 , In summary, either fission yeast or budding yeast could be used as a reasonable model for the study of various viral activities and virus-host interactions.
They often complement to each other in many ways. However, from the evolution perspective, these two yeasts diverged approximately to million years ago 75 , Consequently, both yeasts have homologous genes with higher eukaryotes that they do not necessarily share with each other.
Thus, it is important to know that there are sufficient functional differences between these two yeasts that sometimes could yield conflict results. Similarly, fission yeast has RNAi machinery genes like those in vertebrates, but it is missing from budding yeast Conversely, S.
Another example is that budding yeast has an extended G1 phase of the cell cycle. Thus, the G1-S transition is tightly controlled; whereas fission yeast spends most of its cell cycling time in the G2 phase of the cell cycle.
Hence, the G2-M transition is under tight control. Therefore, the budding yeast might be a better choice to study cell cycle G1-S transition, whereas the fission yeast could serve a preferable role in the study of cell cycle G2-M regulation.
Therefore, careful consideration has to be taken before choosing a model organism to study the viral genes of your interest. In the following sections, special emphasis is given to those studies that have generated significant discovery toward the understanding of a viral function or the virus-host interactions by using either yeast as a model system.
Yeasts have their own indigenous viruses. The fission yeast includes retrovirus-like retrotransposons Tf1 and Tf2 78 , Among those yeast viruses, the dsRNA and ssRNA viruses are infectious, as they are able to infect other healthy yeast cells, and to transmit themselves from cell to cell. As results of the yeast infection, some of those infectious yeast strains kill their receptive cells. Thus, they are also known as killer yeast.
Historically, the final realization that the killer yeasts are actually associated with their own indigenous viruses took more than a century Briefly, Louis Pasteur initially described the contribution of microbes to spoilage of beers in Horace Brown later linked the beer spoilage to Saccharomyces yeasts The killer yeast strains secrete protein toxins K1, K2, K28 and Klus that are lethal to non-killer strains of the same or other species Two dsRNA viruses were subsequently discovered in the killer yeast strains Those two dsRNA viruses are the S.
However, not until , El-Sherbeini and co-workers 12 demonstrated that yeast killer viruses are capable of extracellular transmissions. It was previously thought that killer yeast viruses transmit by cytoplasmic mixing during cell division, mating or other induced forms of cell fusion.
Extracellular transmission was demonstrated by direction infection of K1 and K2 killer viral preparations to yeast spheroplasts, competent yeast cells by lithium acetate, or to mating cells Typically, these two viruses coevolve. An interesting effect of the yeast killing effects is that, besides causing necrosis, they also induce apoptotic programed cell death by triggering caspase- or oxidative stress-mediated apoptosis This apoptotic effects is seen during yeast viral infection of the receptive cells.
Interestingly, however, the killer yeast cells themselves are immune to the toxic effects presumably due to intrinsic immunity Thus, yeasts have been used to study cell apoptosis during virus-host interaction 14 , 15 , 16 , 17 , and to understand potential cellular viral restriction factors toward viral infections 18 , The Gag-Pol fusion protein is produced by a minus-1 -1 ribosomal frameshift during translation, a process that is identical to that used by higher retroviruses Because of the functional similarities of the minus-1 translational ribosomal frameshift between yeast dsRNA viruses and that of higher eukaryotes 92 , it provides a useful tool to delineate molecular actions of viral replication of higher eukaryotic retroviruses such as HIV, which is described in the next section.
A list of higher eukaryotic viruses that are known to replicate in yeast S. Those viruses include plant, animal and human viruses.
By using those sophisticated experimental tools, significant progress has been made in the past several decades to understand the basic aspects of viral life cycle and replication especially those viral steps including translation of viral protein, synthesis of viral genomic template, and association of viral proteins with cellular proteins that are required for viral replication. A number of detailed reviews on these subjects are available 27 , 45 , 46 , 64 , 74 , In the following section, specific examples are given in each of those categories.
This programed translational frameshifting is a viral mechanism to merge proteins encoded by two overlapping ORFs such as Gag and Pol. It is part of a larger three-helix structure of the viral RNA genome.
The stimulatory element and the slippery sequence pairs with an upstream region to form the second helix. Studies on the HIV-1 frameshifting in the yeast S. In particular, yeast viruses such as the ScV-LA virus also use frameshifting to produce its own viral proteins, a process that is identical to that used by higher retroviruses A HIV-1 frameshifting yeast model was first established by Wilson and co-workers who produced the Gag-Pol fragment containing the potential frameshifting site of HIV-1 from a yeast expression plasmid.
In this way, they were able to monitor the production of the frameshifted protein by western blot analysis. Because of the low efficiency of frameshifting events, initially they failed to identify the stimulatory element. Thus, it was believed that no secondary structure was present in the HIV slippery site 98 , However, the stimulatory element was later revealed by NMR A follow-up yeast study by using a dual reporter system indeed confirmed a direct correlation between HIV frameshifting efficiency and presence of the stimulatory element as a stem loop Subsequently, it was shown that a number of retroviruses including HIV-1 have the same stimulatory element.
Together, studies of slippage efficiencies of the HIV frameshifting site in vivo in yeast and in vitro in a mammalian system have demonstrated that this process is essential for viral replication and the molecular mechanisms of frameshifting is conserved from yeast to humans Hence, with in-depth understanding of this -1 frameshifting process, it is possible to design specific antiviral drugs by introducing nonsense mutations.
For example, alteration of frameshifting frequency or artificial introduction of translational stop by a drug during translational frameshifting could either reduce viral infectivity or halt viral replication , Therefore, understanding of the -1 ribosomal frameshifting during translation of viral proteins in yeast provided insights into the molecular mechanism of HIV-1 viral replication.
They all replicate, with various degrees, in yeast Table 1 27 , Geminivirus is the largest Geminiviridae family of plant viruses with more than species. These viruses are responsible for significant crop damages worldwide A geminiviral genome consists of either one or two circular ssDNA in the range of 2, - 3, nucleotides.
Although proteins produced by both viral components are involved in viral replication, only the replication-associated protein Rep is indispensable for viral replication During the rolling circle replication, Rep serves as a multitasking protein. It involves in viral DNA cleavage and joining after one round of replication. It also has ATPase and helicase activities Since some plant cells are terminally differentiated cells, Rep is responsible for reigniting plant cell cycling by pushing cells from cell cycle G1 phase to S phase where cellular DNA synthesis apparatus is reactivated To achieve this goal, Rep binds to plant homologue of mammalian retinoblastoma protein to promote the G1-S transition In this way, Rep reactivates host cell S phase gene transcription and provides a favorable environment for geminivirus replication , , Studies of geminivirus DNA replication in both yeasts have contributed to our understanding toward the initiation of DNA replication in these groups of higher plant viruses.
For example, similar to the role of Rep in plants, the MSV Rep also binds to the maize plant retinoblastoma related-protein pRbR protein as it does in plants This allows in-depth functional analysis of the Rep-pRbR interaction in yeast. Indeed, three nucleotide mutations in the MSV Rep-pRbR interaction motif abolished this interaction in yeast and resulted in significant reduction of MSV-induced symptom severity in maize Interestingly, one of the three mutations C A reversed with high frequency in the maize plant, suggesting the functional requirement and selection pressure of the Rep-pRbR interaction during MSV viral replication.
Similar to budding yeast, Rep showed very similar activities in fission yeast as it does in plants. Furthermore, a RXL motif was identified in the Rep protein that might be an alternative link to the Rep-pRbR interaction and cell cycle control Mutation in this motif abrogated Rep-induced DNA re-replication in fission yeast.
Consistent with the fission yeast finding, the ACMV containing the same mutation in the Rep motif was unable to induce symptomatic infection in tobacco Nicotiana benthamiana plants Genome-wide approaches have been applied to study viral replication of a number of plant, animal and human viruses.
Reviews or reports that cover these topics can be found at 24 , 28 , 46 , The TBSV genome contains five genes that encode a replicase composed of two proteins p33 and p92 , a capsid protein called CP or p41 , a RNA silencing suppressor p19 and a movement protein p22 A number of genomic and proteomic methods were used to identify yeast cellular proteins that are involved in TBSV replication. For a detailed review of this topic, see In brief, a single gene yeast knock-out YKO library was first subjected to a genome-wide screening and revealed 96 genes whose absence either inhibited or stimulated TBSV viral replication Because the YKO library only contains deletions of non-essential genes, additional tests were carried out in a Tet promoter-inducible yTHC library, and a temperature-sensitive ts essential gene library with a total of about genes in each library.
Thirty and additional TBSV replication regulators were found, respectively , A total of proteins were identified. A total of 36 overlapping yeast proteins were identified based on previous screens of other viruses. Consistently, a specific Pkc1p inhibitor, cercosporamide, also resulted in increased TBSV replication in yeast, plant cells, and in whole plants, confirming that Pkc1 and its associated pathways are involved in regulation of TBSV replication Viruses typically encode a limited number of proteins.
They have to rely on host cellular resources to complete their life cycle. Thus, they will take a variety of devious approaches to create a cellular environment for the benefit of their own reproduction One common viral strategy is to subvert host cell cycle into a specific phase of the cell cycle where the virus gains maximal benefit.
After infection, they drive cells to S phase of the cell cycle where the pool of deoxynucleotides is high, thus providing an environment that is conducive to viral DNA synthesis A similar viral action was also noted in ssDNA viruses such as geminiviruses that drive cell cycle G1-S transition , , The possible objective is to avoid competition of cellular resources between the virus and the normal host cellular metabolism Additional benefits to virus-induced cell cycle arrest could include avoiding host antiviral immune responses, maximizing availability of the cellular resources for its transcription, translation and assembly, and delaying programmed cell death until completion of the viral replication , , In the followings, HIV-1 Vpr is used as an example to illustrate how fission yeast was used to delineate molecular mechanism of Vpr-induced cell cycle G2 arrest.
For extensive reviews of this topic, see 63 , 64 , Note that expression of HIV-1 vpr gene in budding yeast resulted in cell growth arrest.
It, however, did not induce cell cycle G2 arrest as it was shown in mammalian and fission yeast cells , , HIV-1 Vpr is a virion-associated viral protein of about Its function is required both in vitro and in vivo for efficient viral infection of non-dividing mammalian cells such as monocytes and macrophages , , It is a multifaceted protein that is involved in multiple steps of the HIV-1 life cycle It involves in cytoplasmic-nuclear transport of proviral integration complex PIC , activates HIV-1 LTR long terminal repeat promoter for viral transcription, and induces cell death through apoptosis In addition, it induces cell cycle G2 arrest in both human and fission yeast cells, suggesting a highly conserved activity of this viral protein , , It was also shown that HIV-1 in cells that arrested in the G2 phase of the cell cycle by Vpr replicates at its maximum level Cell cycle G2-M transition is a tightly regulated cellular process that requires activation of the Cdc2 kinase a human homologue of CDK1 , which determines onset of mitosis in all eukaryotic cells.
HIV-1 Vpr induces cell cycle G2 arrest by subverting the same cell cycle G2-M regulatory apparatus as described above. Subsequent studies in mammalian cells showed that Vpr-induced G2 arrest is mediated through direct binding of Vpr with a Vpr-binding protein VprBP , , which is part of the ubiquitin E3 enzyme, suggesting possible involvement of the ubiquitin proteasome system. Indeed, Vpr associates with the proteasome both in fission yeast and mammalian cells Specifically, in fission yeast, it associates with the 19S subunit of the proteasome through 19S-associated Mts4 and Mts2 proteins.
This VprS proteasome interaction was further confirmed in mammalian cells where Vpr associates with the same two mammalian orthologues Mts4 and S5a of the fission yeast proteins Interestingly, even though both ATM and ATR were shown participating in Vpr-induced G2 arrest, implicating involvement of mitotic DNA damage or DNA replication checkpoint pathways , , neither of these two classic mitotic checkpoint control pathways was exclusively responsible for the G2 arrest induced by Vpr.
Further fission yeast and mammalian studies showed that Vpr induces G2 arrest via a protein phosphatase 2A PP2A -mediated cellular pathway , , Unlike the conventional cell cycle G2-M regulation, Vpr also induces cell cycle G2 arrest at least in part through a mechanism involving in a fission yeast kinase Srk1 and its human homologue MK2 These results suggest that Vpr might modulate cell cycle G2 transition through an alternative and possibly a novel cellular mechanism other than the classic mitotic checkpoints 63 , 72 , Indeed, a later study showed that Vpr induces cell cycle G2 arrest through a unique molecular mechanism that regulates host cell cycle regulation in an S-phase dependent fashion Altogether, this example demonstrates that fission yeast can indeed be used as a reliable model organism to dissect molecular mechanism of HIV-1 Vpr-induced cell cycle G2 arrest.
It was the combined results generated from the fission yeast model system with the study and verification in mammalian cells that led to the finding that Vpr induces cell cycle G2 arrest through a unique virus-mediated cellular mechanism. Viral infection could cause cell death through at least three different ways in yeasts and higher eukaryotes, i.
Necrosis is a form of cell death that is caused by factors external to the cell such as viral infection, which results in the unregulated digestion of cell components. In contrast, apoptosis is a naturally occurring and programmed process of cellular death. Autophagy is a normal cellular process that maintains cellular homeostasis.
It regulates protein degradation and turnover of the destroyed cell organelles. In response to cellular stress such as nutrient starvation or viral infection, autophagy is activated. However, prolonged activation of autophagy often results in autophagy-mediated cell death by either cell necrosis or apoptosis.
Thus, autophagy and cell death are regulated balance of two cellular events. The processes of yeast cell death resemble in many ways those of higher eukaryotes , , , Thus, yeast could serve as model organism to study these terminal cellular processes.
For example, yeast has been used as a model to study yeast necrosis. In contrary to the traditional belief that necrosis is normally a passive cell dying process, evidence accumulated over more than a decade suggests there is actually a regulated necrotic program that controls how long a cell will live longevity or die As for yeast apoptosis, there was long skepticism as whether yeast has true apoptosis.
However, this cynicism starts to dissipate by the increasing evidence generated from yeast studies in the past two decades.
In particular, like in mammalian cells, yeast apoptosis is also mediated through a caspase-mediated proteolytic process in addition to other characteristic apoptotic features , , In fact, some of the same mammalian pro-apoptotic or anti-apoptotic regulators were found in yeasts that show similar activities to higher eukaryotes.
For detailed reviews of this subject, see , , , , , Although yeast apoptosis is not as well studied in fission yeast as in budding yeast, an apoptotic-like process does seem to be present in fission yeast For instance, expression of mammalian pro-apoptotic proteins Bax and Bak induce apoptosis-like cell death that was strongly suppressed by co-expression of the anti-apoptotic protein Bcl-XL , A pombe caspase 1 Pca1 was identified and its budding yeast homologue Yca1p was shown to be a bona fide caspase Moreover, both caspase-dependent and -independent processes are present in fission yeast , Therefore, at least some of the mammalian apoptotic processes are present in yeasts.
Such yeast-mediated apoptosis typically occurs at low-to-moderate concentration of viral toxins in those cells; whereas necrotic cell death takes place at high concentration, suggesting activation of apoptotic or necrotic cellular death regulators requires different thresholds of stimuli.
Expression of exogenous viral proteins also induce cell death and apoptosis in yeasts 64 , Anti-apoptotic viral proteins include baculovirus p35 and DPV protein of the Deerpox virus In the followings, we present two HIV-1 viral proteins Vpr and PR as examples to demonstrate how studies on virus-mediated yeast cell death and apoptosis were carried out in budding and fission yeast. HIV-1 PR is an essential viral enzyme. Its primary function is to proteolyze the viral Gag-Pol polyprotein for production of viral enzymes and structural proteins as well as for maturation of infectious viral particles.
HIV-1 PR induces apoptosis in mammalian cells by caspase-3 cleavage and interruption of mitochondrial functions , Interestingly, however, HIV-1 PR kills budding yeast resulting in cell lysis; whereas no cell lysis was observed in fission yeast. The difference between these two yeasts could potentially be explained, at least in part, by the relative thicker cell wall of fission yeast than budding yeast , Studies in the fission yeast further demonstrated that HIV-1 PR cleaves its indigenous viral protein target sequences such as matrix and p6 proteins , Moreover, PR-induced cell death triggered the reactive oxidative species ROS production, an indication of oxidative stress.
It also caused changes in mitochondrial morphology that are linked to apoptosis 67 , Significantly, Hhp2 kinase suppressed, at least in part, HIV-1 PR-induced cell death and apoptosis in mammalian cells Vpr also induces cell death in budding and fission yeast , Further characterization of Vpr-induced cell death in budding yeast showed that the C-terminal domain of Vpr is primarily responsible for the cell killing effect in yeast and mammalian cells , When the C-terminal Vpr was subject to intact mammalian cells or purified mitochondria, it induced apoptosis through a permeability transition pore complex PTPC of mitochondria Consistently, yeast strains lacking part of the PTPC showed reduced Vpr-induced killing than the wildtype control cells.
Similar to Vpr-induced apoptosis in mammalian cells, Vpr triggers ROS production, promotes phosphatidylserine externalization and induces hyperpolarization of mitochondria in fission yeast, leading to changes of mitochondrial membrane potential These data suggested that HIV-1 Vpr-induced cell death in fission yeast is reminiscent of apoptosis. A novel anti-apoptotic protein, translational elongation factor 2 EF2 was isolated It not only suppresses Vpr-induced cell death in fission yeast but it also suppresses Vpr-induced apoptosis in mammalian cells through caspase 9 and caspase 3-mediated mechanism 66 , As described in the previous sections, yeasts have proven to be fruitful hosts to conduct genome-wide studies on virus-host interactions, particularly because their small genomes and genetic amenability.
For the same token, yeast could also, in principle, serve as a surrogate to carry out functional study of small viral genomes. It is conceivable that effects of single or multiple viral gene products could be tested separately or simultaneously in the same yeast strain, thus allowing testing the same basic cellular function that is affected by individual or combination of different viral proteins.
Besides all of the operational and genetic advantages of using yeast as a model organism, a large-scale gene cloning strategy and a streamlined functional characterization system are also needed for this purpose. Example of such a fission yeast system is shown in Fig. Please note that there is nothing new in the molecular features of these shuttle vectors.
Goal of Fig. Thus, notable features of this fission yeast system include 1 the gene cloning process is streamlined to a sequential order to add or remove the green fluorescent protein GFP tag. Top the pYZ1N vector contains a wild type nmt1 promoter 68 , It carries a LEU2 gene for selection. Unique cloning sites in these vectors are indicated. Adapted from 36 , Note that nothing is new in molecular features of shuttle vectors described.
Goal of this figure is to illustrate a robust and streamlined strategy of shotgun gene cloning of a small viral genome. In a genome-wide and functional analysis of the HIV-1 genome in fission yeast, each one of the HIV-1 genes was cloned and expressed individually in a wild type fission yeast strain As a result of this type of replicative cycle, appearances of cold sores and genital herpes outbreaks only occur intermittently, even though the viruses remain in the nervous tissue for life.
Latent infections are common with other herpes viruses as well, including the varicella-zoster virus that causes chickenpox. Chicken pox virus : a Varicella-zoster, the virus that causes chickenpox, has an enveloped icosahedral capsid visible in this transmission electron micrograph. Its double-stranded DNA genome incorporates into the host DNA and reactivates after latency in the form of b shingles, often exhibiting a rash.
Plant viruses can cause damage to stems, leaves, and fruits and can have a major impact on the economy because of food supply disruptions. As plant viruses have a cell wall to protect their cells, their viruses do not use receptor-mediated endocytosis to enter host cells as is seen with animal viruses.
This damage is often caused by weather, insects, animals, fire, or human activities such as farming or landscaping. Additionally, plant offspring may inherit viral diseases from parent plants. When plant viruses are transferred between different plants, this is known as horizontal transmission; when they are inherited from a parent, this is called vertical transmission. Symptoms of viral diseases vary according to the virus and its host. One common symptom is hyperplasia: the abnormal proliferation of cells that causes the appearance of plant tumors known as galls.
Other viruses induce hypoplasia, or decreased cell growth, in the leaves of plants, causing thin, yellow areas to appear. Still other viruses affect the plant by directly killing plant cells; a process known as cell necrosis. Other symptoms of plant viruses include malformed leaves, black streaks on the stems of the plants, altered growth of stems, leaves, or fruits, and ring spots, which are circular or linear areas of discoloration found in a leaf.
Oak tree galls : Galls are abnormal plant growth or swellings comprised of plant tissue. Galls are usually found on foliage or twigs. These unusual deformities are caused by plant growth-regulating chemicals or stimuli produced by an insect or other arthropod pest species. The chemicals produced by these causal organisms interfere with normal plant cell growth.
Plant viruses can seriously disrupt crop growth and development, significantly affecting our food supply. They are responsible for poor crop quality and quantity globally, and can bring about huge economic losses annually. Other viruses may damage plants used in landscaping. Some viruses that infect agricultural food plants include the name of the plant they infect, such as tomato spotted wilt virus, bean common mosaic virus, and cucumber mosaic virus.
In plants used for landscaping, two of the most common viruses are peony ring spot and rose mosaic virus. There are far too many plant viruses to discuss each in detail, but symptoms of bean common mosaic virus result in lowered bean production and stunted, unproductive plants. In the ornamental rose, the rose mosaic disease causes wavy yellow lines and colored splotches on the leaves of the plant. Privacy Policy. Skip to main content. Search for:.
Virus Infections and Hosts. Steps of Virus Infections Viral infection involves the incorporation of viral DNA into a host cell, replication of that material, and the release of the new viruses. Learning Objectives List the steps of viral replication and explain what occurs at each step. Key Takeaways Key Points Viral replication involves six steps: attachment, penetration, uncoating, replication, assembly, and release. During attachment and penetration, the virus attaches itself to a host cell and injects its genetic material into it.
During release, the newly-created viruses are released from the host cell, either by causing the cell to break apart, waiting for the cell to die, or by budding off through the cell membrane. Key Terms virion : a single individual particle of a virus the viral equivalent of a cell glycoprotein : a protein with covalently-bonded carbohydrates retrovirus : a virus that has a genome consisting of RNA.
The Lytic and Lysogenic Cycles of Bacteriophages Bacteriophages, viruses that infect bacteria, may undergo a lytic or lysogenic cycle. Learning Objectives Describe the lytic and lysogenic cycles of bacteriophages.
Key Takeaways Key Points Viruses are species specific, but almost every species on Earth can be affected by some form of virus. The lytic cycle involves the reproduction of viruses using a host cell to manufacture more viruses; the viruses then burst out of the cell. The lysogenic cycle involves the incorporation of the viral genome into the host cell genome, infecting it from within. Key Terms latency : The ability of a pathogenic virus to lie dormant within a cell.
Animal Viruses Animal viruses have their genetic material copied by a host cell after which they are released into the environment to cause disease. Learning Objectives Describe various animal viruses and the diseases they cause.
Key Takeaways Key Points Animal viruses may enter a host cell by either receptor -mediated endocytosis or by changing shape and entering the cell through the cell membrane. Viruses cause diseases in humans and other animals; they often have to run their course before symptoms disappear. Residual viral proteins that remain within the cytoplasm of the host cell can be processed and presented at the cell surface on MHC class-I molecules, where they are recognised by T cells.
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