Definitions Flashcards
(188 cards)
1
Q
anthropogenic inputs to oyster habitats:
A
contaminants/run off – generate novel compounds that persist in the environment, combustion of fossil fuels – contributing to global warming, ocean acidification and deposition of metals – impact physiology and biochemistry of native species.
2
Q
Assumptions in transcriptomics/differential expression studies:
A
For one, assuming changes in mRNA lead to changes in the proteome and subsequent changes in metabolic processes. While increases in some mRNAs do not lead to the subsequent change in the proteome, globally/generally, there is ample evidence to show that changes to mRNA lead to changes in the proteome (87% of protein levels in yeast were correlated w mRNA levels). There is also experimental validation for the relationship between gene expression and metabolic phenotypes/outcomes.
3
Q
Oyster response to hypoxia:
A
Oysters close their shells which prevents oxygen exchange with the environment. This causes a rapid change in internal pH due to accumulation of CO2 from aerobic respiration and the acidic end products of anaerobic metabolism. This leads to a build up if acid (metabolic acidosis). Moderate decreases in pH support metabolic rate depression, this is the main adaptive mechanism in surviving extreme stressors in intertidal molluscs. At extreme low pH the oyster mobilizes calcium carbonate stores in their connective tissues and shell to buffer intra and extracellular pH. Restoring the acid-base homeostasis can contribute to oxygen debt which is a strong increase in oxygen demand during post-anoxic recovery.
4
Q
Indels:
A
insertion-deletion polymorphism. A mutation where 1-100 kb nucleotides are inserted or deleted from DNA. These can occur in coding and non-coding regions.
5
Q
Frameshift variant:
A
Where a single nucleotide or group of nucleotides are inserted or deleted from a DNA sequence that causes a shift in th reading frame which disrupts the normal triplet reading of DNA. This misread leads to a different product.
6
Q
aragonite saturation state
A
aragonite saturation state is a measure of carbonate ion concentration, decreases in carbonate ion concentration means an increase in acidification. High wind events can advect deep more acidic water on to shallow shoals causing a decrease in aragonite saturation state and reducing growth and degrading shells.
7
Q
Phenotypic plasticity:
A
the ability of an organism to produce distinct phenotypes to environmental variation. This phenotypic variation impact various systems and aspects of an organism including morphological, physiological and behavioral changes.
8
Q
Neo-Darwinism:
A
This is an evolutionary theory where genetic variation and natural selection drive evolutionary change, with phenotypes being more fixed. This theory is contrasted by phenotypic plasticity where a genotype can express multiple phenotypes in response to the environment. These changes can be heritable but generally are not considered heritable.
9
Q
Discrete phenotypic variation
A
, is more binary in nature and results in alternate phenotypes this is also known as polyphenism. Ex. color or form of insects depending on what season development took place in.
10
Q
Continuous phenotypic variation
A
is difficult to identify in the environment because it’s hard to pin down causality. An example would be plant growth in response to light availability. It would be difficult to tease this apart in nature among other factors like water and nutrient availability. Shell thickness in response to predator presence (good oyster example).
11
Q
Adaptive traits:
A
‘positive’ traits. Traits developed in response to environmental conditions that help it survive when faced with a new environment. These traits help or contribute to evolution.
12
Q
Non-adaptive traits:
A
Environmentally induced changes that push the species away from the optimal phenotype. Traits like these develop in response to extreme environmental stress. While they’re initially unhelpful they can also increase the variance around the mean expressed phenotype due to expression of cryptic genetic variation that could facilitate adaptive evolution by chance.
13
Q
Conditional regulation of phenotypic plasticity:
A
phenotype expression is regulated by the presence or absence of an environmental condition.
14
Q
Stochastic regulation of phenotypic plasticity:
A
multiple phenotypes are expressed even when the environmental conditions are controlled.
15
Q
Genetic polymorphism:
A
the presence of 2 or more variant forms of a specific DNA sequence that occur among different individuals or populations. SNPs are most common. A SNP is classified as variation at a single nucleotide among more than 1% of a population. Depending on the frequency of a SNP it can be used to distinguish populations, individual susceptibility to disease, among other traits.
16
Q
The difference between genetic polymorphism and environmentally induced polyphenism:
A
Environmentally induced polyphenism aka discrete phenotypic variation is a type of developmental phenotypic plasticity. This is when a specific discrete phenotype (like color) is expressed in response to the environment. Genetic polymorphisms are underlying and not changed by the environment. They can impact the degree of plasticity an individual or population may have, but they do not change in response to the environment.
17
Q
Canalization:
A
robustness/developmental stability of a genotype to produce a phenotype despite environmental conditions aka trait is no longer plastic. Would produce a flat reaction norm plot.
18
Q
Genetic assimilation
A
process by which a phenotypic character, initially produced in response to environmental pressure, becomes taken over by the genotype so it’s formed regardless of environmental influence. (Sommer, 2020) This results in a loss of plasticity (canalized) (Ghalambor et al., 2007)
19
Q
Genetic accommodation
A
A type of genetic assimilation. This is a mechanism of evolution where a novel phenotype (by environment or mutation) is refined into an adaptive phenotype through quantitative genetic changes but doesn’t necessarily lead to a loss of plasticity.
20
Q
Hormesis:
A
an adaptive biphasic dose response where lower doses provide protective effects that can lead to improvement in organism performance, while higher doses cause detrimental effects that has fitness and performance consequences.
21
Q
Adaptive response:
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A plastic response aimed at restoring homeostasis.
22
Q
Preparation for the oxidative stress hypothesis:
A
a strategy for animal adaptation to harsh environmental conditions. Reactive oxygen species signal that resuming normal metabolism would come with more reactive oxygen species damage, this activates cellular defenses in preparation.
23
Q
Within generation carryover effects
A
Phenotypic changes from a previous life stage experience that impact a later stage. These can be positive or negative.
24
Q
Phenotypic plasticity:
A
the ability for an underlying genotype to express multiple phenotypes based on environmental conditions. Can be developmental or liable.
25
Developmental phenotypic plasticity:
a form of plasticity that focuses on the ability to adjust the phenotype to the environment during development/ontogeny.
26
Liable phenotypic plasticity:
Allows an organism to maintain homeostasis under stress throughout their lifespan by helping to resist the loss of basic function during rapid environmental changes.
27
Selective Mortality:
non-random mortality of individuals with unfavorable phenotypes and underlying genotypes that are disadvantageous during bouts of environmental stress. This is generally beneficial to wild populations with high degrees of genetic diversity, but it can be of concern with hatchery reared populations. Selective mortality decreases genetic diversity and hatcheries by nature already have lower genetic diversity than wild populations. There for in a hatchery, selective mortality can further limit genetic diversity and effective population size which increases the likelihood for inbreeding depressions and emergence of lethal mutations.
28
fecundity
Cost of fertilization is different from cost of larvae production. Estimates of larval mortality that contrast (organisms’ reproductive capacity/how many offspring it can produce) [Larval Ecology, General Knowledge] with settlement may overexaggerate larval mortality because it doesn’t account for poor fertilization. It’s hard to establish rates of fertilization. Larval mortality rates in species with external fertilization tend to be overestimated for this reason.
29
internal fertilization and release of larvae:
Larval release is timed with many environmental factors (light-dark cycle, tidal & tidal amplitude cycle, lunar cycle). Synchronous hatching may promote larval survival. Night hatching reduces encounters with visually feeding fish. Hatching during low tide would keep larvae close to reefs and shorelines. High tide would promote transport away from adults.
30
6 sources of physiological stress:
variable temperature and salinity, low DO, pollution, UV radiation, and poor nutrition.
31
How stress effects development:
stressed larvae may develop abnormally due to needing to reallocate energy to survival rather than development (Schatz et al., 2024). This can disrupt rates of change during tightly coordinated development events. Additionally the effects of stress particularly from variable environmental conditions, can depend on species. Larval tolerances are generally a match for the geographic range of the species. In the case of oysters this is probably more localized.
32
Mortality due to temperature fluctuation
generally occur in northern/southern limits of the species distribution, shallow margins of bays or estuaries (marshes, mangroves, seagrass beds), near the beginning/end of reproductive seasons.
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neustonic larvae
Ozone depletion may reduce survival of (those that inhabit the uppermost layer of the water column)
34
Primary pelagic predators of larvae
planktivorous fishes and gelatinous zooplankton (hydromedusae, scyphomedusae, ctenophores). Others include decapod larvae, siphonophores, chaetognaths, copepods, hyperiid amphipods, euphausiids and shrimp.
35
Hydromedusae
one of the most important predators. They’re small so they target small prey. They occur in aggregations and have high feeding rates. The pierce soft-bodied larvae or use nematocysts
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Scyphomedusae
large voracious predators of zooplankton. Large swarms in the summer. They prefer zooplankton over invertebrate larvae.
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Ctenophores
high clearance rates, eat a wide variety of invertebrate larvae. Mnemiopsis leidyi depresses zooplankton populations during summer blooms and is negatively correlated with larval abundance and recruitment. Prey on oysters (Kennedy et al., 1996).
38
Benthic invertebrate predators of larvae
Also grasp but also suspension feeders. Larvae encounter these predators when they hatch, undergo vertical migrations in shallow water, or settle.
39
buccal suction
Primarily use vision and (rapid expansion of the mouth and throat (buccal cavity) to generate suction to pull prey into mouth) to detect and capture prey.
40
Morphological defenses against predation:
nematocysts, spicules, setae, spines, shells, and mucus. Transparency and small body size also reduces visibility and detection. Most obvious in the oyster would be their shell they develop. Ability to survive through the guts of some predators like scyphomedusae.
41
Behavioral defenses against predation:
akinesis, shadow response, negative rheotaxis. Flairing of setae, spines or arms. Horizontal migration from areas with high predator densities. Diel vertical migration where fish are prevalent and reverse vertical migrations from where invertebrate predators are prevalent. Releasing gametes when predators are inactive or dormant. Oyster larvae may avoid settling near high densities of predators (Pruett and Weissburg, 2019).
42
Akinesis:
a lack of movement that serves as camouflage making them harder to spot and catch. Common in polychaete and crab larvae.
43
Shadow response:
responding to a sudden decrease in light by sinking or escaping. Common in polychaete and crab larvae.
44
Negative rheotaxis:
moving away from a current as a defense mechanism to avoid other planktonic predators that get carried with the current. Common in invertebrate larvae.
45
Chemical defenses against predation:
secreting chemicals to make larvae unpalatable. Chemical recognition of species’ own larvae to avoid cannibalism.
46
Larval advection:
the transport of larvae via hydrodynamics Lavae regulate their hydrodynamic transport by timing, duration, and amplitude of vertical swimming relative to tidal cycles (in estuaries).
47
Larval dispersal patterns in estuaries
retention within the estuary (oysters?), export from estuaries with subsequent reinvasion, and invasion of larvae from coastal waters with subsequent export of juveniles or adults.
48
Determination of settlement location:
Settlement of larvae is well studied. determined by a combination of large- and small-scale hydrodynamics and larval response to chemical cues, water velocity or depth.
49
Differential DNA methylation regions:
altered DNA methylation patterns that are associated with transgenerational epimutations. These are specifically propagated through the male germline. Implies the mechanism of epimutation is similar to that of imprinted genes. There are proven connections between DMRs, altered mRNA transcriptome and adult onset phenotypes but questions on specifics of this mechanism may lie in non-coding RNAs. If ncRNAs that regulate gene expression (both pre and post transcriptional levels) fall within this region, it could have wide spanning effects on genes distributed through out the genome.
50
imprinted genes
(genes where only one copy (maternal or paternal) is expressed, and the other is epigenetically silenced. These genes stay silenced through the waves of reprogramming and remain that way permanently).
51
Non-coding RNAs (ncRNA):
stretches of RNA that do not code for a specific protein but play a vital role in regulating gene expression and other cellular processes. They have multiple molecular means to participate epigenetic transgenerational inheritance. Initially divided by size large (lncRNA) >200 nt and small (sncRNA) <200 nt, there are finer classifications.
52
Large intergenic ncRNA (lincRNA):
not located within protein-coding genes. lincRNAs can function as epigenetic regulators by interacting directly with epigenetic factors involved in epigenetic modification (like chromatin remodeling, DNA methylation, histone modifications, or epigenetic memory). They can also function indirectly by affecting transcription or translational activity or affecting the stability of mRNAs encoding epigenetic factors. lincRNAs are often transcribed close to the genomic regions they’re destine to regulate. They can also serve as sequence guides that attract complexes that remodel chromatin or other epigenetic machinery.
53
Polycomb group protein complexes (PGC)
a family of protein complexes that can remodel chromatin and induce epigenetic silencing of genes.
54
Pre-pachytene piRNA or MIWI2-piRNA
a subclass of sncRNA exclusively expressed in polycomb-group protein complexes that are required for remethylation after reprogramming of male germ cells and for the maintenance of hypermethylation in many imprinted genes, making it a likely candidate for perpetuating epimutations induced by environmental factors. Post-transcriptional level.
55
Transposons:
segments of DNA that can move from one location in a genome to another. “Jumping genes”
56
miRNA:
microRNA, regulate mRNA stability and translational efficiency. Post-transcriptional level
57
Endo-siRNA:
endogenous small interfering RNA, regulate mRNA stability and translational efficiency. Post-transcriptional level.
58
Promoter-associated RNA (PAR):
bind to promoter regions of mRNA and function as transcriptional activators by interacting with transcriptional machinery. Pre-transcription level.
59
Enhancer RNA (eRNA)
transcribed from enhancer regions of DNA bind to promoter regions of mRNA genes and function as transcriptional activators by interacting with transcriptional machinery. Pre-transcription level.
60
Heterochromatin formation:
an epigenetic process where chromatin is compacted into a highly condensed state, silencing gene expression.
61
Hypermethylation of DNA:
epigenetic process where methyl groups are added to a DNA molecule which changes the activity but not the sequence of the DNA segment. This epigenetic process modulates gene expression.
62
Repressive histone modifications:
chemical changes to histone proteins that silence or active transcription.
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Ways ncRNAs facilitate formation of epimutations:
ncRNAs can initially form these epigenetic modifications through interacting directly with epigenetic factors, regulating epigenetic states by affecting transcriptional or translational activity, by affecting the stability of mRNAs encoding for epigenetic factors, by acting as attractants or “sequence guides” for epigenetic machineries, they can also have distal effects in an epigenetic control region, where alterations have cascading effects on target genes both close and distant.
64
DNA methylation:
the enzymatic addition of a methyl group to a cytosine residue in DNA. Supporting enzymatic machinery includes maintenance methyltransferase and de novo methyltransferases. The regulatory role (repressor, more common or activator) of DNA methylation is specific to the genomic context.
65
Maintenance methyltransferase (DNMT1):
copies preexisting methylation patterns to the new strand during mitosis.
66
De novo methyltransferase (DNMT3A/3B):
establishes DNA methylation patterns.
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How DNA methylation represses gene expression:
when present in the promoters of genes DNA methylation typically represses expression through physically blocking transcription factors or through associations with DNA-binding proteins.
68
How DNA methylation promotes gene expression:
When DNA methylation is located in the gene body it’s associated with high levels of expression.
69
Histone variants:
different histones that can be post-translationally modified which alters the degree of chromatin compaction and play an important role in mediating responses to environmental cues.
70
Chromatin:
dynamic structure that supports both the packaging of the genome into the nucleus and the regulation of genes via changes in DNA accessibility. The basic repeating structure of chromatin is the nucleosome. Chromatin can enhance or repress transcription by changing it’s structure. These chromatin states can be inherited both mitotically and meiotically.
71
Nucleosome:
The basic repeating structure of chromatin that consists of DNA wrapped around an octamer of four core histone proteins. High order chromatin structures are established by linker histones between nucleosomes.
72
Lamarckism:
an evolutionary theory, where physical changes acquired through-out an organism’s lifetime can be transmitted to their offspring. This theory is still regarded as incorrect, but aspects of Lamarckism are present in the modern understanding of epigenetics.
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Histone proteins:
small, basic proteins that are key structural elements. They facilitate the packing of long eukaryotic DNA within the limited space of the nucleus. This mechanism also modulates the accessibility of different regions of the genome.
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Nucleosome:
histones in octamers associated with DNA. The fundamental subunit of chromatin.
75
Histone variants:
diversification of histones into different families that encompass functionally specialized groups. Some of these groups have been identified as being critical to epigenetic regulation.
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Histone H2A.Z:
the most studied histone variant due to its involvement in maintaining genome integrity.
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Histone posttranslational modifications:
acetylation, methylation, phosphorylation, etc (more than 10 types but those are the most notable). These modifications participate in the regulation of chromatin structure, help recruit proteins and chromatin-remodeling complexes that influence DNA processes (transcription, repair, replication, recombination). They also play critical roles in chromatin metabolism and epigenetic memory.
78
Acclimatization:
short-intermediate timescale cellular response of an organism to changing biotic and abiotic conditions.
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Phenotypic plasticity:
the capacity for an organism to display a variety of phenotypes as a function of the environment. Two scales, intragenerational plasticity and transgenerational plasticity.
80
Intergenerational plasticity:
generated by signals occurring within an organism’s life. Effects range from transient to enduring results. Types include reversible acclimatization and development acclimatization.
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Reversible acclimatization:
acclimatization that facilitates beneficial outcomes but is short-term and doesn’t endure far beyond it’s initiator.
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Developmental acclimatization:
signals from the developmental environment set a trajectory toward a phenotype in anticipation of such conditions later in life. Like a signal passed from mom to offspring to trigger a change during development that induces a phenotype that is supposed to help them upon being born. Thickness of fur coat in meadow vole. Also common in marine calcifiers in response to ocean acidification.
83
Transgenerational plasticity:
induced by signals set prior to fertilization that modulate the offspring reaction norms in different ways. Majority of aquatic invertebrates show positive transgenerational plasticity where exposure of parental generation to adverse conditions induces protective effects in subsequent generations. A mechanism for this would be transgenerational epigenetic inheritance.
84
Codon bias:
is the preferential or non-random use of synonymous codons. Codon bias varies with species, and also between genes within an organism.
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Epigenetic biomarkers
can be defined as any epigenetic mark or altered epigenetic mechanism that is stable and reproducible during sample processing and can be measured in the body fluids or tissue preparations.
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primary miRNAs:
long, capped, polyadenylated RNA molecules transcribed by miRNA genes. First step in the biogenesis of miRNAs.
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Drosha:
an RNA-specific ribonuclease, part of the microprocessor complex responsible for cleaving pri-miRNA into pre-miRNA.
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Precursor-miRNAs:
hairpin RNAs 60-100 nt that are transported from the nucleus to the cytoplasm for additional processing.
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Dicer:
RNase III endonuclease found in the cytoplasm that processes pre-miRNAs into double stranded RNA.
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RNA-induced silencing complex (RISC):
turns double stranded RNA into miRNA and guides it to it’s mRNA target.
91
Hyper
and Hypomethylation of CpG islands: if it occurs in the promoter region of miRNA genes, it represses miRNA gene expression. Hypomethylation activates miRNA expression
92
Histone Modification a
cetylation example: Reducing deacetylation relaxes chromatin and promotes miRNA expression which in turn can regulate it’s targets, while increasing deacetylation compacts chromatin and reduces miRNA expression and thus cannot regulate it’s targets.
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Methylation:
addition of a methyl group (CH3). Affects function. Well studied modification of histone residues. Has more complex effects on miRNA regulation. Methylation of certain targets may upregulate certain miRNAs while downregulating others.
94
Acetylation:
addition of an acetyl group (CH3CO). A major post-translational protein modification. Acetyl-CoA (metabolite) donates the acetyl group, to the alpha-amino group at the N-terminus (amine end) of the protein. Well studied modification of histone residues. In terms of lysine, acetylated lysine relaxes chromatin and increases gene expression while deacetylation of lysine compacts chromatin and decreases gene expression.
95
Ubiquitylation:
covalent attachment of ubiquitin (small protein) to a substrate protein. Controls critical cellular events like cell cycle progression, cytokine signaling and immunity.
96
Phosphorylation:
addition of a phosphoryl (PO3) group to a molecule. Common in conversion of ADP to ATP (oxidative and substrate-level)
97
Sumoylation
post-translational modification that conjugates small ubiquitin-like modifiers (SUMO) to lysine residues of target proteins. Alters molecular interactions of the target by masking or adding interaction surfaces.
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Biotinylation
covalent attachment of biotin to a protein, occurs in carboxylases (group of proteins).
99
ADP-ribosylation:
post-translational modification of adding one or more ADP-ribose. Inversely related to transcription.
100
miRNA-epigenetic feedback
loop: regulates cell processes like cell proliferation, apoptosis and differentiation.
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miRNA seed sequence region
the first 2-8 nt beginning from the 5’ to the 3’ these must be complementary to the target mRNA UTR 3’. Important in miRNA targeting as they act as recognition motifs.
102
Cross generational plasticity:
adult conditioning involving one generation of germ line cells (F0 (parent) to F1 (offspring))
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Multigenerational plasticity:
more than one cycle of germ line development involved (F1 (offspring, probably their gametes, 2 cycles of germ line development)-F2 and beyond).
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Carryover effects:
Phenotypic changes from a previous life stage experience that impact a later stage.
105
Primordial germ cell
development: precursor to germline cells (sperm and eggs). These cells are formed via preformation or continuous germ cell specification. After formation they’re protected by migration and sequestration. Sequestration is usually achieved through physical location protecting them from somatic differentiation signals. Knowledge on PGC specification timing, type of sequestration, and duration of inactive state is important for testing cross- and multi-generational plasticity.
106
Preformation primordial germ cell specification:
Development of primordial germ cells through early specification by maternally inherited determinants. This occurs when germ cells are sequestered in germ plasm cytoplasmic regions. Components of the germ plasm target the cells, initiate specification and then inactivate. When primordial germ cells are inactive, environmental influence is unlikely.
107
Continuous primordial germ cell specification:
An inductive mechanism common in diverse taxa. Development of primordial germ cells occurs in early life stages and possibly through the adult stage driven by cell-cell signaling. Epigenetic reprogramming of somatic cells clears most epigenetic modifications prior to germ line development (?)
108
Phenotypic modulation
graded and continuous response.
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Developmental conversion and threshold traits
discrete switches in phenotype with no intermediate version.
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Environmental cue vs stimuli:
cues are non-harmful stimuli that predict environmental change or threat (I.e. oysters reacting to the chemicals in crab pee is a predator cue, not harmful but predicts a nearby threat). Environmental stimuli is a harmful selective agent like high temperature, low DO, etc. the line between these is blurred and persistent indicators of environmental stimuli should eventually evolve into cues. Both stimuli and cues can originate internally or externally.
111
Examples of
polyphenism: alternative polyphenism in social insects. Workers, soldiers and reproductive castes all arise from the same genotype, environmental factors affect hormone titers and trigger developmental switches that alter gene expression (Klowden, 2008).
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Anticipatory Phenotypic Plasticity:
individuals initiate phenotypic change before the appearance of a harmful (or beneficial) environmental factor.
113
Responsive Phenotypic Plasticity:
individuals initiate a phenotypic change after the appearance of a new environment or changed environmental factor. This may result in damage before the individual changes.
114
Active environmentally induced phenotypic change:
the response requires multiple regulatory genes and processes acting at different hierarchies to produce a complex and coordinated change. Example: diapause/dormancy in insects (do oysters exhibit diapause in the winter?). Diapause is often anticipatory, if phenotypic plasticity is active and anticipatory it’s a strong indicator of adaptive plasticity. Note that most forms of plasticity will have aspects of both active and passive plasticity.
115
Passively induced environmental phenotypic change:
susceptibilities to physical or chemical environmental stress that result in passive changes to the phenotype not regulated by the organism. Example: poor nutrition leading to small size. Note that most forms of plasticity will have aspects of both active and passive plasticity.
116
Period of Responsiveness:
When a species can respond to environmental change varies greatly. Some can produce plastic responses throughout their lives, some only during certain developmental windows. Example: arthropods have specific windows of opportunity due to their discrete life stages and external skeleton. Changes can’t be made after shell formation.
117
Physiological homeostasis:
maintenance of an equilibrium state by some self-regulating capacity (Debat & David, 2001). Therefore, homeostasis is the act of manipulating physiology in response to monitoring of internal and external conditions. Some homeostatic mechanisms and phenotypic plasticity have similar physiological mechanisms. Physiological homeostasis requires an underlying plasticity.
118
Evolution of plasticity via susceptibility:
environmental change disrupts physiological homeostasis and uncovers phenotypic variation. Changing environment and biochemical conditions may disrupt repression of pieces of the genome that can better cope with the altered environment. Useful combinations of new traits would be selected for and more plastic individuals would survive and go on to reproduce.
119
Evolution of plasticity via exaptation:
When a previously existing plasticity comes to serve a new function or is induced by a new cue or is otherwise shifted in it’s expression.
120
Interchangeability:
A key concept to understanding the evolution of phenotypic plasticity. Traits are genetically and environmentally influenced. Example melanin, and end product of well described enzyme chains, coded in DNA, but also environmentally influenced. Cold temp, more melanin, darker skin, more solar heating. The control is evolutionarily interchangeable. When there is genetic variation for degree of environmental influence, natural selection can select for increased or decreased environmental sensitivity. Regulation of many traits is downstream of DNA so new phenotypes only require repatterning of genetic architecture and epigenetic interaction.
121
A
dditive variance: the deviation from the average phenotype due to inheritance of a particular allele and this allele’s relative effect on the phenotype. This is a sub-category of genetic sources of variation which is a component for calculating phenotypic variance.
122
Genetic variance:
is the amount of variance that is a result of genetic sources of variation. The subcategories of genetic variance are additive, dominance, and epistatic variances. Genetic variance is a component for calculating phenotypic variance.
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Dominance variance:
variance due to interactions between alternative alleles at a specific locus. Think about heterozygosity in dominant vs recessive alleles. Aa if the A is dominant produces a dominant phenotype. If there is no dominance an Aa phenotype would be a mixture of the AA and aa phenotypes.
124
Epistatic variance:
also involves an interaction between alleles but these alleles are associated with different loci. If a trait like color is first influenced by another trait, like presence or absence of pigment, that is located on another loci.
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Phenotypic variance
is the result of genetic sources of variation (genetic variance) and/or environmental sources (environmental variance).
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Heritability:
a measure of the proportion of phenotypic variance that is attributable to genetic variance. This is an indicator of if a population can respond to natural or artificial selection.
127
Environmental variance:
The amount of environmental variation responsible for a particular phenotypic trait. The subcategories are specific environmental variance, general environmental variance, and genotype by environment interaction.
128
Specific environmental variance:
the deviation from the population means due to the environmental conditions that are experienced by each individual. This is an error or residual variance metric. This is determined by the variation within replicated genetic lines.
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General environmental variance:
the nongenetic sources of variation between individuals that are experienced by multiple individuals in a population. Usually, the largest component of variance in populations under natural conditions. This is determined by the variation of replicated genetic lines in each natural or experimental environment of interest.
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Bet hedging strategies:
long term fitness is maximized across generations by producing offspring with different characteristics to increase the chances of survival in unpredictable environmental conditions. Examples include egg or seed banks (accumulation of long-lived diapausing eggs), dormancy, temporal dispersal or migration.
131
Polygenic quantitative traits:
influenced by multiple gene genetic that ultimately contribute to a phenotype. They don’t follow mendelian inheritance patterns due to this polygeny and often associated with continuous traits rather than discrete ones, though some discrete traits are polygenic.
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Single locus traits:
determined by a single gene at a specific locus on a chromosome. Predicted using mendelian inheritance principles like dominance and resistiveness.
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Reciprocal phenotypic plasticity:
when phenotypic change in one individual induces change in another
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Adaptive plasticity:
adaptive plasticity is a reaction norm that results in the production of a phenotype that is in the same direction as the optimal value favored by selection in the new environment. Adaptive plasticity can result in the conversion of non-heritable environmentally induced variation to heritable variation (Ghalambor et al., 2007)
135
Genotype x Environment Interaction:
variation among genotypes in how they respond across environments (Ghalambor et al., 2007). This is visualized by plotting the reaction norms of multiple genotypes GxE interactions.
136
When does natural selection favor adaptive plasticity:
when (given genetic variation) populations are exposed to variable environments, those environments produce reliable cues, selection favors different phenotypes in each environment, and there’s not one phenotype that has optimal fitness across all environments.
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Fixed development:
requires only production machinery (structural genes, polymerases, ribosomes, etc.). This gives rise to an expected phenotype (mean phenotype with variance).
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Plastic development:
can be very similar to fixed development (allelic sensitivity) but more often it involves many steps (sensing cues, processing information, inducing regulatory mechanisms, creating and inducing production machinery) that offer opportunity for costs or limits to arise.
139
Cost of plasticity
when in an altered environment, the plastic organism displays lower fitness than the fixed organism while producing the same mean trait value. Five categories: Maintenance costs, information acquisition cost, developmental instability, and genetic costs
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Maintenance costs:
the energetic cost of maintaining additional sensory and regulatory mechanisms that would not be necessary in a fixed organism. Ex: sensory machinery to sense an environmental cue.
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Production cost:
Some debate over what defines a production cost. The paper DeWitt et al defines it as a cost of plasticity when the cost of production is greater for plastic phenotypes than for fixed genotypes when producing the same phenotype.
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Information acquisition cost:
the cost of collecting information about the environment.
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Developmental instability:
within generation phenotypic variance for a given genotype or deviation from the optimal phenotype over time. If there’s too much variance in a phenotype among a population they’ll have lower fitness than a population with little variance and a narrow distribution. But empirical evidence suggests these two are unrelated phenomena. Often the correlations do not hold up across traits or environments.
144
Genetic costs:
Three types of genetic costs, 1. linkage where genes with plasticity are linked to costly genes for other traits, 2. Pleiotropy plastic genes also confer negative direct effects on other traits, 3. Epistasis plastic genes alter the expression of other genes and indirectly effect other traits.
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Limit of plasticity:
when plasticity in response to the environment cannot produce a trait mean as close to the optimum as the fixed development can.
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Information reliability limits:
the reliability of information collected may be variable if an environmental cue is unreliable or isn’t well interpreted by the organism leading to poor phenotype-environment match up.
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Lag-time limits:
lag time between the cue and the environmental impact can have an adverse effect on the effectivity of plasticity. Can be mitigated by using indirect cues (if reliable). Behavioral or physiological plasticity reacting to a short-term/short-lived altered environment can have minimal lag time, while lag time can have a big effect on something like induced morphological traits that are developing over an extended period of time.
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Developmental range limits:
A trade off between range of expression (many variations across a wide range of ecosystems) and magnitude of expression (ability to create extreme phenotypes). Fixed development is more likely to give rise to extreme phenotypes. Ex. a plant fixed for long stems could produce a longer stem than their plastic counterparts in an altered environment where long stems are preferred.
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Epiphenotype
problem: A phenotype built as an add-on may not be as good as one integrated into development. Ex. zooplankton growing a spine on an existing carapace rather than a spine integrated into the carapace in development.
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Putative binding site
a binding site on a molecule that is suspected to be where another molecule binds but it has not been proven
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Restriction endonucleases
can be used to cleave DNA molecules at particular sites by recognizing specific sequences. Different restriction enzymes result in different cut positions and different sized fragments of DNA
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Hybridization
, taking advantage of the capacity for denatured DNA to reanneal and producing base pairing between complementary single-stranded polynucleotides.
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Next Generation Sequencing:
technology for determining the sequence of DNA or RNA to study genetic variation associated with biological phenomena. NGS is different from previous versions like Sanger sequencing because it enables sequencing of many DNA strands at the same time.
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Sanger sequencing
the “chain termination method” precursor to NGS. Processes a single strand at a time. Uses PCR and gel electrophoresis to determine original sequence.
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dNTPs and
ddNTPs: dideoxyribonucleotides (ddNTPs) are chain terminating and used to stop the extension of oligonucleotides at random during the first step of sanger sequencing. dNTPs are modified nucleotides with unique fluorescent labels and used during chain formation in the first step of sanger sequencing.
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Paired-end libraries:
These libraries have adaptor tags on both ends of the DNA fragments. This enables the fragment to be sequenced from both directions. This provides value during sequencing data reconstruction.
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Single reads:
short, sequenced fragments. These can be joined by using overlapping regions into a continuous fragment. This continuous fragment assembled by putting together single reads is called a contig. It’s a continuous sequence.
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Paired end reads:
the same size as single reads but they come from opposite ends of DNA fragments that are too long to be sequenced all the way through. Knowing paired end reads were generated from the same piece of the sequence can help link contigs into scaffolds. Paired read data can also indicate the size of repetitive regions and how far apart contigs are.
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Contig:
a continuous stretch of sequence (DNA or RNA) based on where read fragments overlap and the order of bases is known with a high degree of confidence. Focused on local overlap and read comparison.
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Scaffold:
ordered assemblies of contigs with gaps in-between representing regions of unknown sequence. Scaffolding orients and orders contigs using the reads and linked information. Scaffolding methods can use chromosomal spatial patterns to order contigs.
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De novo assembly:
an assembly approach that assumes no prior knowledge of the sequence length, layout, or composition. De novo assembly is a lot more complicated, requires higher sequencing depth, and computationally intensive than mapping to a genome. A potential advantage is that you’re not relying on a reference genome so if the quality of the reference genome is very poor or missing large stretches of sequences, de novo assembly is done completely independent of that reference genome. Uses overlapping regions to connect fragments therefore fragments need to be pretty long. Appropriate to use when a reference genome isn’t available or isn’t of high quality, when identifying novel regions.
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Microarrays
a tool used to detect the expression of thousands of genes at the same time. DNA microarrays are microscope slides that are printed with thousands of tiny spots in defined positions with each spot containing a known DNA sequence or gene. Also known as gene chips.
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miRNA
UTR method: miRNAs suppress gene expression by binding to the 3’ untranslated region (3’ UTR) and inducing mRNA degradation.
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miRNA
CDS method: By binding to the coding sequence (CDS) portion of the gene, this represses gene expression by inhibiting translation.
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Heat Shock Proteins
(HSPs) are in charge of proteostasis (the cellular process of maintaining proper balance, structure and function of proteins within an organism) and buffering stresses. They are a molecular chaperone (proteins that assist other proteins in folding properly, refolding after denaturation and preventing aggregation). Specifically, they maintain correct folding of polypeptide chains and assembly of the protein complex. HSPs can be regulated by co-chaperones.
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Hox genes
are major regulators of animal development. They define patterns of development. They’re crucial for embryonic development. In oysters, they’re not one contiguous block, but four sections with non-Hox genes interspersed. They also show temporal non-collinearity, or disruption of temporal collinearity, which is just a fancy way to say the timing of their activation doesn’t follow the normal sequence dictated by their physical position along the chromosome.
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Apoptosis
(programmed cell death) helps fight viral, parasitic, and bacterial infections. It’s a highly conserved form of regulated cell death and it’s mediated by two major pathways. An extrinsic death-receptor mediated pathway and an intrinsic mitochondrial pathway.
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I
nhibitor of Apoptosis Proteins (IAPs): regulate cell death pathways by directly or indirectly inhibiting caspases (enzymes that breakdown proteins), regulating ubiquitin (Ub, a small protein that tags other proteins for degradation)- dependent signaling events via E3 ligase (enzyme that catalyzes the joining of two molecules) activity, and mediating activation of the pro-survival NF-kB pathway.
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signal transduction pathway
A is a pathway by which a signal is passed.
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Larval mortality:
mortality that occurs after fertilization or hatching but before settlement.
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Low fertilization
and Larval Mortality: low fertilization can reduce larval settlement but eggs that are not fertilized are not considered larvae and therefore don’t contribute to larval mortality. Though it’s difficult to tease these apart in practice.
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Factors that regulate spawning success in oysters:
presence of spawning stimuli (increasing water temp, algal ectocrines), synchronized spawning (males spawn in response to general egg pheromone, females species-specific sperm pheromone (logical because eggs are viable for shorter period than sperm)), presence of microbial grazers, nutritional status of females and their eggs. (Kennedy et al., 1996 pg 357)
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Oyster s
pawning stimuli: increasing water temperature. Chemical stimuli – algal ectocrines, spawning triggered by a chemical released by phytoplankton. Serotonin is an important neurotransmitter involved in the spawning process of males, used to stimulate spawning in aquaculture. Salinity does not appear to play a role in stimulating spawning but salinities <6 ppt can inhibit gametogenesis
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Contributors to s
ynchronized spawning: Male oysters are more responsive to spawning stimuli and the presence of sperm stimulates females to spawn. The active component in sperm that triggers females to spawn is species-specific but in eggs the active component that stimulates males to spawn is common to eggs of other bivalves (Kennedy et al., 1996, pg 357). Additionally, a density of 30,000 eggs/L optimal concentration for successful fertilization in hatchery.
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Sex specific v
iability of gametes: Sperm stays viable for up to 5 hours, eggs became non-viable an hour after separating from ovarian tissue. This makes synchronized spawning incredibly important. (Kennedy et al., 1996, pg 35X)
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Contributions of spawning to surrounding environment:
Ingestion by microheterotrophs. oyster sperm are ingested by microprotozoans and support protist growth. Estimated that over half of all sperm released in a salt marsh could be consumed by microbial grazers in 24 h.
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Nutritional status of females
and effect on reproduction: eggs contain lipid and protein reserves and the number of eggs released and quantity of nutrients in the yolks of those eggs is dependent on nutrition of females. Sublethal environmental factors can inhibit gametogenesis.
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Contributors to larval mortality:
Duration of larval period (longer planktonic period, increased probability of predation and advection from suitable settlement habitat. Stress can disrupt development and rates of change during tightly coordinated development events (Schatz et al., 2024). Larval stress tolerances are generally matched to geographic range of the species. Sources of physiological stress include temperature, salinity, dissolved oxygen, pollution, UV, poor nutrition.
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Morphological defenses against predation:
nematocysts, spicules, setae, spines, shells, and mucus. Transparency and small body size also reduces visibility and detection. Most obvious in the oyster would be their shell they develop. Ability to survive through the guts of some predators like scyphomedusae.
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Behavioral defenses against predation
akinesis, shadow response, negative rheotaxis. Flairing of setae, spines or arms. Horizontal migration from areas with high predator densities. Diel vertical migration where fish are prevalent and reverse vertical migrations from where invertebrate predators are prevalent. Releasing gametes when predators are inactive or dormant. Oyster larvae may avoid settling near high densities of predators (Pruett and Weissburg, 2019)
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Akinesis:
a lack of movement that serves as camouflage making them harder to spot and catch. Common in polychaete and crab larvae.
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Shadow response:
responding to a sudden decrease in light by sinking or escaping. Common in polychaete and crab larvae.
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Negative rheotaxis:
moving away from a current as a defense mechanism to avoid other planktonic predators that get carried with the current. Common in invertebrate larvae.
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Chemical defenses against predation
secreting chemicals to make larvae unpalatable. Chemical recognition of species’ own larvae to avoid cannibalism.
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Oyster-specific m
orphological defenses against predators: transparency and small body size reduce visibility and detection. The shell oysters develop protects them from predators and also enables them to survive through the gut of some predators like scyphomedusae (though as previously mentioned the medusae are not major predators of oyster larvae).
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Oyster-specific b
ehavioral defenses against predators: oyster larvae may avoid settling near high densities of predators (Pruett & Weissburg 2019).
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Hormesis:
an adaptive biphasic dose response where mild stress results in protective effects that can lead to increased organismal performance while high doses of stress lead to detrimental effects that lead to poor performance and fitness (Barry & Lopez-Martinez, 2021).
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Adaptive response:
a plastic (flexible) response aimed at restoring homeostasis after exposure to stress.
