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HBIO405 Evo Med Exam #1 > Development > Flashcards

Development Flashcards

1
Q

development and phenotype

A

-All cells have virtually the same genotype but each cell type will express a specific gene so the phenotypes are different
-Developmental process can also contribute to phenotype and therefore evolution

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2
Q

cell fate

A

“normal development” without any interference

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3
Q

definition of potency and its 4 levels

A

potency: range of cell types it can give rise to
Totipotent: this cell can turn into all of the cells in the human body
Pluripotent: this cell can form any cell in the human body except embryonic membranes
Multipotent: can give rise to diverse cell types within a specific tissue
Unipotent: cells can only divide and give rise to one cell type

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4
Q

definition of differentiation

A

overt morphological changes that accompany or follow commitment/determination(which means it is in a set direction of what it will become)

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5
Q

final differentiation

A

last step, results in unipotential cell that will follow the same fate for the rest of its life

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6
Q

embryonic and post embryonic development

A

Embryonic development: all major organ systems established (first 8 weeks)
Post embryonic development: growth and refinement of such systems (post 8 weeks)

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7
Q

development and its 5 steps

A

a single cell gives rise to a mature organism
1. cell proliferation
2. cell growth
3. differentiation
4. pattern formation
5. morphogenesis

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8
Q

development and cell proliferation

A

is cell division and is controlled by the constant cycle of cell death (apoptosis) and proliferation
Ex: hands start as flat but cell death in between where fingers will be creates fingers

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9
Q

Hypertrophy vs Hyper plasticity

A

cell division and growth cycles
Hypertrophy: is overgrown cells that are larger than they should be which causes thickness
Hyper plasticity: tissue has excessive proliferation of cells, so the large number of cells causes the thickness

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10
Q

differentiation and development

A

cells acquire new structural, functional, and morphological characteristics so they become new cells which is unidirectional so go only one way (exception of cancer)
- Cells choose to express certain genes so they can acquire distinct identities
- Transcription factors determine what the cell’s identity will be (gene expression) and are controlled by signaling processes

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11
Q

development and pattern formation

A

cells become organized into tissues, organs, & organ systems where an initial body plan is formed first

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12
Q

development and morphogenesis

A

organs and other morphological characteristics take shape and use many different mechanisms to do so; differential cell proliferation, selective cell-cell and cell-matrix adhesion, changes in cell shape/size, apoptosis

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13
Q

cell differentiation

A
  • Cell differentiation is done through a series of irreversible hierarchical decisions
  • As development continues cells become more differentiated so they lose potency
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14
Q

3 step process of cell differentiation

A
  1. Induction: specific signals (mechanical, chemical, biological) change the behavior (fate, differentiation, morphology …. etc.) of a cell or group of cells
    - Competence: is the ability for a cell to respond to signaling
  2. Commitment takes place when: a cell has received a signal that promotes differentiation towards a specific lineage
    (Not to be confused with cell fate where an environment change can affect the fate of the cell)
  3. Determination: cell has received signals or absence of additional cues so it is irreversibly committed to differentiation into a specific lineage, (usually involving specific transcription factors)
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15
Q

Terminal Differentiation

A
  • A cell can no longer differentiate into another cell type and often can no longer proliferate
  • Ex: heart cells cant proliferate so once they die you can’t get more so results in heart failure
  • Can be associated with permanent changes in DNA
    -DNA methylation or other epigenetic mechanisms
    -genetic rearrangements like Beta cells rearranging immunoglobin (Ig) genes so they can only form 1 type of Ig
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16
Q

lineage

A

genetics
- what cell did that cell arise from

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17
Q

position

A

environment
invertebrates can develop distinct stereotypic phenotypes as a result of developmental influences; polyphenism
-example: female bee larva feeds on royal jelly it turns into queen but if not it will be a regular worker bee

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18
Q

cell fate depends on lineage and position because……

A

Lineage determines a cell’s potency
Position determines the developmental cues a cell is exposed to (induction if signals are from nearby cells)

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19
Q

embryonic development timeline

A

Days 7-14: initial division
Day 14: gastrulation, three distinct tissues form endo, ecto, mesoderm
Days 19-21: Neurulation, begins nervous system and brain
Days 21-24: beginning of future head, neck, mouth, nose
Weeks 3-8: organ formation begins
Week 8: fetus formed

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20
Q

first trimester

A
  • Zygote travels through fallopian tube and implants in wall of uterus (endometrium)
  • Develops: organs, limb buds, facial features, placenta
  • Especially vulnerable to teratogens (factors affecting growth) at this time
  • Miscarriage most likely often due to chromosomal abnormalities
  • Placenta provides nutrient via umbilical cord
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21
Q

Embryology and development process

A

-Fertilization: 2 haploid gametes fuse to make 1 diploid individual
-Sperm nucleus merges with nucleus of oocyte to make the zygote
-A day later mitotic division takes place until the Morula is formed
-At 16 cell Morula stage it undergoes compaction so 2 types of cells
- At 32 cell stage cavitation occurs and the blastocoel (fluid filled cavity) forms and on one side the nonpolarized cells form the inner cell mass which will become the embryo
-They blastocyst attaches to uterine wall at day 6/7

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22
Q

compaction

A

-Is the 1st differentiation
- membrane polarization
- Process where cells go from loosely arranged to tightly packed with tight junctions to stabilize it and then it starts reorganizing so that there is a recognized inside and outside to the cell
- Internal nonpolarized cells (inside cell) gives rise to embryo
- External polarized cells (outside) will give rise to placenta and extra embryonic membranes

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23
Q

Gastrulation

A
  • Blastula turns into Gastrula when specific cells migrate inwards (mesendoderm)
  • Produces 3-layer embryo
    1. Endoderm: forms epithelial inner linings of organs
    2. Mesoderm: forms most system of the body like skeletal and muscular plus more
    3. Ectoderm: forms epidermis and central nervous system most importantly plus more
  • Cells in the inner cell mass produce a bilaminar embryo, and the layer facing away from the blastocoel will give rise to the embryo through gastrulation
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24
Q

cavitation

A

the blastocoel (fluid filled cavity) forms and on one side the nonpolarized cells form the inner cell mass which will become the embryo

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25
Q

neurulation

A

-Neural plate folds into neural tube which gives rise to brain and spinal cord
-Ectoderm invaginates to give rise to spinal cord and brain and skin
-Neurulation induces the development of the mesoderm into different organs and body parts
-The surface ectoderm produces growth factors that stimulates the growth of other organs

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26
Q

second trimester

A

-continued growth and maturation
-3 inches to about a foot long by end of 2nd trimester
-Some premature fetuses (born @ end of 2nd trimester) survive with intensive neonatal care
-Brain makes up ½ of embryo in fetal development stage

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27
Q

third trimester

A
  • Intense growth and maturation
  • Fetus gains ½ to ¾ its weight
  • Increased brain growth (extensive)
  • Lungs fully mature (last organ to mature)
  • Liver matures later than most organs
  • Rapid increase in body fat storage
  • A balance diet is critical for the mother
28
Q

reaction norm

A

range of phenotypes that can form under diff condition in it’s environment
- Genetic predisposition + environmental factors = phenotypic traits (particularly important in fetal development)

29
Q

developmental plasticity

A

an embryo has the ability to differentiate and adapt its phenotype from its genotype in response to its environment and stimulus
This links evolution and development
Good: provides reproductive fitness, adaptable to external environment, ex: fetus stays small and diverges nutrients to important parts if its exposed to starvation
Bad: cells and tissue are very sensitive to external factors, ex: retinoic acid affect babies but not adults, fetal alcohol syndrome
- Some taxa developmental plasticity can give rise to different morphologies but humans it’s a range of phenotypes, ex: alligator eggs over 34 degrees is male and under 30 degrees is female

30
Q

stabilizing selection

A

tendency to select against extreme phenotypes and select closer to the average
so the bulk of variation is clustered around the average phenotype which reduces genetic diversity

31
Q

canalization

A

consistency of phenotypic traits so traits are similar among all subjects

32
Q

developmental plasticity is a key factor of evolution because ………

A
  1. During fetal development it allows one to adapt to its environment
  2. Enhances fitness and adjusts regulatory processes
  3. It’s during a time that is intermediate between selection and homeostasis
33
Q

Types of Developmental Plasticity

A
  1. Altered anatomy
  2. Altered physiology- ex: babies born on cold places have fewer sweat glands and more brown adipose and inverse for hot places
  3. Altered behavior
  4. Altered life history traits- island effect
34
Q

Allocation, differentiation, proliferation of embryonic stem cells can be determined by 3 environmental factors

A

Nutrition environment – fatty acids mean more adipose
Endocrine environment – hormones
Chemical environment – alcohol

35
Q

Fetal Origin Hypothesis

A

the period of gestation has significant impacts on developmental health and well being outcomes for individuals ranging from infancy to adulthood

36
Q

thrifty genotype hypothesis

A

-Started as thrifty genotype hypothesis by James Neel in 1962
-where a certain genotype is efficient at storing nutrient in the form of fat
- Many nonwestern peoples exposed to nutrient abundance were more prone to metabolic dysfunctions like diabetes and mismatch principle
- Revised hypothesis: thrifty phenotypic Hypothesis

37
Q

what happens to a fetus developed in a nutrient scarce environment ?

A
  • it develops adaptations to live in a nutrient scarce environment
  • so it redirects energy into crucial organs (heart/brain) and diverts from others (adipose)
  • when exposed to nutrient abundance later in life its at an increased risk to develop chronic conditions due to metabolic dysfunctions
  • malnourished fetuses had focused energy to more important organs so they have underdeveloped adipose tissue so as an adult when calories increase drastically the triglycerides cant be stored in adipose because they are underdeveloped so the triglycerides have to be stored in other places like the liver and heart
38
Q

thrifty phenotype results in

A

increased risk for developing chronic illness (related to metabolic dysfunction, stroke, coronary heart disease, diabetes, hypertension

39
Q

Island Effect

A

Homo floresiensis remained stuck on an island so it experienced insular dwarfing because of nutrient scarcity selecting for a smaller sized person because smaller size is easier to sustain, shorter gestation, earlier puberty/maturity, childhood phase shorter because less nutrients

40
Q

Expandability Theory

A

-Adipocyte number is a major detriment of fat mass, it entirely relies on pre-adipocytes formed perinatally or during puberty because preadipocytes cant proliferate during adulthood
-# and location of preadipocytes determines the definitive body fat capacity and distribution
-Adipose tissue has a limited maximal capacity to increase in mass while safely storing fat
-When adipose tissue reaches its expansion limit it will fail as a storage organ for triglycerides, so lipids start to be deposited into non-adipose organs where they exert lipotoxic effect (can cause cell death)
-Lipids start depositing in skeletal muscle and liver where they can disrupt insulin resistance
-Lipids deposit into arteries so it contributes to atherosclerosis
-Over filled adipose cells can cause inflammation

41
Q

Arguments Supporting Expandability Theory

A

-(Lipodystrophies are) disorders of dysfunctional adipose tissues is associated with metabolic dysfunctions
-Some morbidly obese people who present with a favorable metabolic profile (10%) do so because they are hyperplastic morphology which can store triglycerides without causing inflammation
-TZDs stimulate adipose tissue development (proliferation)

42
Q

TZDs stimulate adipose tissue development :
- how they work
- what they treat

A

1.Commonly used to treat nonalcoholic fatty liver disease because it creates increased space to store triglycerides
2.they work by promoting adipose tissue expansion to accommodate excess lipids
3.Treats type 2 diabetes to make you fatter by increasing the number of fat cells which decreases insulin resistance associated with inflammation

43
Q

Hyperplastic Adipose Tissue

A

-Increase in fat cell # (proliferation)
-Early onset (juvenile)
-Excessive nutrients and calories ingested during critical times for fat cell numbers to increase are last trimester, first year of life, puberty
-80% have difficulty losing weight because the mass is in the large cell number, and you can never reduce the number of fat cells you have

44
Q

Hypertrophic Adipose Tissue

A

-Increase in fat cell size
-Adult onset
-Increased fat intake later in life increases fat cell size when fat storage exceeds fat release
-Can lose weight easily because mass is in the fat cells size not in the number of fat cells

45
Q

gestational diabetes

A

excessive nutrient abundance during development causes insulin resistance & hyperinsulinemia, affecting fetal glucose metabolism and adiposity

46
Q

Hyperleptinemia

A

excessive nutrient abundance during pregnancy may reduce leptin sensitivity thus stimulating adiposity

47
Q

Diabetes

A

blood glucose is unable to enter muscle and adipose cells Because insulin function is impaired
-Diabetes can also cause:
cardiovascular disease like heart attack and stroke. neuropathy, nephropathy, & retinopathy
-People don’t die of low glucose levels because we have artificial insulin but die of high glucose levels b/c of insulin resistance

48
Q

what are 4 things insulin does in the body?

A

regulates blood glucose metabolism and is necessary for adipose cells and striated muscles to import glucose into cells
1. Stimulates translocation of glucose transporters in most insulin resistant cells (adipose tissue and skeletal muscle)
2. Regulates glucose metabolism: increase glucose uptake and catabolism, decrease glucose synthesis
3. Insulin enhances utilization of amino acids: increase protein synthesis, decrease protein catabolism
4. Insulin promotes fat synthesis and decrease fat catabolism

49
Q

relationship between insulin, glucose, glucagon

A

-Ingest food = increase glucose so increase insulin to counterbalance the increases in glucose
-Large concentration of glucose can damage cells
-Glucagon is an antagonist to insulin, low glucagon when fed, high glucagon when fasting

50
Q

Type 1 Diabetes

A

-Insulin production in the pancreas is partially or completely impaired
-Could be caused by an autoimmune reaction toward Beta cells
-Glucose disposal is delayed
-Lose weight

51
Q

Type 2 Diabetes

A

-Insulin production works but become insulin resistant
- Initially the pancreas compensates by producing more insulin
- Eventually the pancreas fails to produce enough insulin
- Muscle and adipose tissue cells don’t respond to insulin
- Glucose disposal is delayed
- Can’t treat with insulin
- Gain weight
- Evolution explanation: having a little insulin resistance is good because we used to starve more so gestational diabetes is still prevalent so that the baby has glucose leftover for it

52
Q

What happens with maternal metabolic dysfunction ?

A

-Mother has hyperglycemia and hyperinsulinemia so baby is exposed to both and becomes accustomed to hyperinsulinemia because of the increased insulin concentration the baby becomes insulin resistant
-Baby has increased risk for developing T2DM and obesity later in life and into adulthood

53
Q

leptin
- function
- factors

A

-Leptin is an adipokine (signaling molecule secreted by adipocytes)
-Leptin is produced in white adipose tissue and is the peripheral signal for central nervous system for satiety
-Leptin functions as a setpoint for the brain to control energy intake & expenditure so that a constant amount of adipose tissue is maintained
-Function of leptin: promotes satiety, stimulates fat catabolism (lipolysis), inhibits insulin secretion, stimulate glucose metabolism in muscle and liver (burn calories), increase energy expenditure (thyroid function which stimulates metabolism)
-Leptin depends on many factors: adiposity determines serum leptin production, sex (higher leptin in women), higher leptin in subcutaneous fat, insulin production increases leptin

54
Q

parabiosis

A

2 mice are stitched together by blood vessels, the skinny mouse produced leptin which then transferred through the blood vessels into the fat mouse and made the fat mouse lose weight

55
Q

Leptin and obesity
- mechanism

A

-Obese people have increased leptin production and therefore develop resistance to leptin
-mechanism for leptin resistance is unknown but may have to do with impaired leptin signaling in brain which could be caused by inflammation in hypothalamus

56
Q

maternal obesity and leptin

A

-obesity during pregnancy causes increase of leptin which then effects the regulation of appetite and metabolic homeostasis in the fetus
-hyperleptinemia during pregnancy can lead to leptin resistance in the fetus which can have long term implications for the offspring
-this all promotes the cycle of obesity because it can be inherited by future offspring

57
Q

developmental disruption

A

-extreme cases of developmental plasticity
-environment can disrupt development (teratogens) by interfering with processes of: gene expression, cell proliferation, differentiation, migration &morphogenesis
-some disorders: neural tube defect, fetal alcohol syndrome, phocomelia

58
Q

neural tube defects (NTD)
- causes
- environmental factors
- genetic factors

A

-caused by failure of neural tube to fold during neurulation
-folate is necessary for nucleotide synthesis
-the inability to produce nucleotides causes a delay in closure of neural tube
-if neuroepithelial cells don’t have enough nucleotides, cellular replication slows and neural folds formation is retarded
-NTDs have multifactorial of causes and exact mechanism by which folate is implicated is unknown
- environmental factors: maternal illness (diabetes) or nutritional deficiencies(low folate), maternal infection(Zika), drugs (alcohol)
-genetic factors: mutations on MTHFR gene

59
Q

neural tube defects and folate

A

folate is a vitamin so we can’t produce it and must ingest it so to optimize it our body recycles it back into folate and is turned into three key nucleotides of thymine, adenine, guanine.
exact mechanism by which folate is implicated is unknown

60
Q

neural tube defect disorders
anencephaly
craniorachischisis
iniencephaly
encephalocele
spina bifida

A

anencephaly: no brain
craniorachischisis: neural tube doesn’t close
iniencephaly: missing tissue so neck is stuck looking up
encephalocele: a bunch of neurons stuck outside brain
spina bifida: closed or open cysts on baby’s tail bone spine area

61
Q

spina bifida and it’s 4 types

A

-is way milder than other NTD
-severity of NTD depends on the extent of spinal cord involvement
-occulta: vertebrae is slightly deformed
-meningocele: meninges sticks out but the nerves stay inside
- meningomyelocele: nerves and meninges sticks out
-Myeloschisis: nerves are sticking out and separates the meninges

62
Q

Neural tube disorders

A

-Have multifactorial causes and the mechanism involving folate is not completely understood
-severity of NTD depends on the extent of spinal cord involvement !!
-If neuroepithelial cells don’t have an adequate internal supply of nucleotides then cellular replication slows down therefore the development of the neural folds is retarded
-Folates are key in the construction of ¾ main nucleotides so important for neurulation
-Along with folate other deficiency of riboflavin, PLP, and cobalamin have been linked to neural tube defects

63
Q

Fetal Alcohol Syndrome - general concept

A
  • When alcohol crosses the placenta the fetus doesn’t have a fully formed liver so it can not detox the ethanol and acetaldehyde which disrupts fetal development
  • Affects the neuronal plasticity which disrupts brain development and function
64
Q

Fetal Alcohol syndrome Causes

A
  1. Characteristic facial anomalies
  2. Growth retardation
  3. CNS involvement (cognitive impairment, learning disabilities, behavioral abnormalities)
65
Q

Features of Fetal Alcohol syndrome

A

mental retardation, behavior impairment, attention deficit, epicanthal folds (extra skin that hides the pink inner corners of the eyes), thin upper lip, hypoplastic nose (small nose), micrognathia (jaw is smushed backwards on face), smooth philtrum

66
Q

thalidomide

A

-Greatest modern medical tragedy
-Used to treat morning sickness and was usually safe with few side affects
-In reality it causes severe fetal malformations because it’s a teratogen
-Fetal exposure to thalidomide causes phocomelia
-Phocomelia: limb malformations due to the interference with blood vessel formation
-Can be used as a chemotherapeutic treatment because it stops the formation of blood vessels so the cancer can’t get new nutrient supply from new blood vessels

67
Q

Discovery of insulin

A

Banting and Best injected insulin into a beagle named Mary who had no pancreas and kept her alive with it and now used it on a child to help him live

HBIO405 Evo Med Exam #1 (7 decks)

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