Human Bio FINAL

goals of male reproductive system

1. make sperm/semen

2. deposit sperm as close o the cervix as possible

testes

site of sperm production which occurs in the seminiferous tubules

sperm cell

• haploid

• acrosome- contains enzymes used during fertilization

• lots of mitochondria for energy

• flagellum- tail for swimming

seminal vesicle

produce watery fluid with fructose and lipids

prostate gland

contributes an alkaline compound to neutralize acidity of vagina

bulbourethral gland/cowper’s gland

make pre-ejaculate fluid to aid sperms exit from body

semen

combination of mature sperm and the fluids from accessory glands that leave body at ejac.

penis

delivers sperm near cervix

hormone regulation

1. hypothalamus secretes GnRH (gonadotropin releasing hormone)

2. Anterior pituitary releases gonadotropins (FSH and LH)

3. Gonads (testes and ovaries) release hormones that assist reproduction and feedback to brain

   • testosterone, estrogen, progesterone

FSH in males

made in anterior pituitary gland

• stimulates seminiferous tubules to produce sperm

LH in males

produced by the anterior pituitary

• stimulates leydig cells to make more testosterone

testosterone

made in the Leydig cells

• stimulates anterior pituitary and many other targets in body to produce primary and secondary sex characteristics ad regulate negative feedback for sperm and testosterone production

Goals of female reproductive system

1. make an egg that is available for fertilization— ovaries

2. create a suitable environment for the embryo/fetus to develop if egg is fertilized— uterus

ovarian cycle

• increased level of FSH made by ant. pituitary causes maturation of an ovarian follicle (primary—> secondary)

• surge in LH also made by anterior pituitary causes ovulation and formation of corpus luteum

primary follicle

composed of oocyte and follicle cells

secondary follicle

composed of oocyte, antrum, and follicle cells

• produces estrogen

corpus luteum

formed from empty secondary follicle

• produces progesterone and estrogen

• degenerates if no pregnancy occurs

uterine cycle

mature follicle in ovary makes estrogen—> thickening the endometrium

corpus luteum in ovary makes progesterone and estrogen—> causes further thickening and maintenance of endometrium

FSH in females

made by the anterior pituitary

• causes primary follicles to mature into secondary follicles

estrogen

made by the corpus luteum, primary follicle, placenta

• stimulates endometrium to thicken and anterior pituitary to release LH

LH in females

made by the anterior pituitary

• stimulates secondary follicle to become corpus luteum and triggers ovulation

Progesterone

made by the corpus luteum and placenta

• thickens the endometrium and stops the release of FSH and LH from ant. pituitary

GnRH

made by the hypothalamus

• triggers release of gonadotropins (FSH/LH) from the anterior pituitary

Pregnancy

embryo makes HCG

• maintains corpus luteum to maintain estrogen and progesterone levels and endometrium thickness

After implantation, placenta takes over making hCG and eventually estrogen and progesterone to maintain endometrium as well

no pregnancy

degeneration of corpus luteum leads to decreased estrogen and progesterone= shedding of endometrium and beginning of new cycle

PCOS

hormonal imbalance causes overproduction of androgens such as testosterone which prevents maturation of follicles

endometriosis

endometrial tissue grows outside the uterus

fertilization: Sperm

1. sperm is ejaculated into a woman’s vagina to the cervix

   • cervix must be open

   • sperm can be trapped in folds of cervix

2. sperm swim through cervix and uterus to the correct fallopian tube

   • pass through think cervical mucus

   • bypass immune cells in female that attack sperm

fertilization: Egg

1. woman releases one egg from one of the two oviducts per month

   • 50% chance sperm enter correct tube

   • sperm swim against current created by cilia

2. sperm that reach egg compete to penetrate protective layer

   • only one sperm will enter egg to complete fertilization

   • occurs in the fallopian tube

sexual reproduction

• involves two organisms

• gametes are produced by the organisms

• offspring show genetic variation

• gametes are produced by meiotic and mitotic divisions

asexual reproduction

• involves one parent

• gametes are not produced

• offspring are genetically identical to parent

• cell division is ONLY mitotic

somatic body cells

divide by mitosis

germ cells

divide via meiosis

• spermatocytes and oocytes

meiosis

meiosis 1

1. prophase 1- homologs pair up and crossing over occurs by swapping regions of DNA

2. metaphase 1- homologs line up next to one another in center of cell

3. anaphase 1- homologous chromosomes separate and are pulled toward opposite poles

4. telophase 1- nucleus reforms, cells are now haploid

Meiosis 2

1. prophase 2- cells from meiosis 1 continue into meiosis 2 without interphase or DNA replication

2. metaphase 2- chromosomes line up in single file in middle of cell

3. anaphase 2- sister chromatids separate

4. telophase 2- nucleus reforms resulting on 4 daughter cells

mitosis vs. meiosis

mitosis

• 1 round of cell division

• no recombination/ crossing-over

• preserves chromosome # (start and end w 46)

• daughter cells are diploid and identical to parent cell

Meiosis

• 2 rounds of cell division

• recombination/crossing over

• start with diploid cell (46) end with haploid cell (23)

• daughter cells are different from parent

non-disjunction

chromosomes fail to separate from one another leading to inheriting more than 2 copies of a chromosome

trisomy

3 copies of the same chromosome inherited instead of 2

• causes 47 chromosomes instead of 46

• trisomy 21= down syndrome (extra chromosome on 21)

monosomy

only one chromosome of a pair is inherited

• inheritance of 45 chromosomes instead of 46

• usually fatal except Turner Syndrome (XO)

3 things in meiosis that contribute to variation

1. recombination during prophase 1

2. independent assortment in metaphase 1

3. reduction of chromosome content to half of original

independent assortment

random sorting of chromosome versions during gamete formation

gene

observable physical feature like hair or eye color that’d determined by production of a particular protein

allele

particular form of a gene, blue vs green eyes

• homozygous- alleles for gene are the same version on homologous chromosomes

• heterozygous- alleles for gene are different versions on homologous chromosomes

homologous chromosomes

one member of each pair is inherited from each parent

look alike (size, shape, banding pattern, genes)

alleles are NOT identical

locus

location of a specific gene on a chromosome

genotype

individuals complete set of alleles

phenotype

observable physical and functional traits, hair color, blood type, disease susceptibility

• determined by inherited alleles and environmental factors

dominant allele

masks the complimentary allele

recessive allele

will not influence the phenotype if paired with dominant allele, must be paired with another recessive allele

incomplete dominance

heterozygous phenotypes is intermediate between that of either homozygote

• heterozygote children will have inbetween phenotypes (example one parent has straight hair HH and the other has wavy hair hh= child with wavy hair Hh)

codominance

products of both alleles are expressed and contribute to phenotype

• AB blood type (A and B carbs on RBC surface)

polygenic inheritance

inheritance of phenotype traits thats depend on many genes. Usually distributed within a population as a continuous range of values

• most human genes are not determined by a single gene or allele

empirical law

based on data gathered by original experiments or observations, the truth about events, NO interpretation (Newton’s law of motion)

scientific theory

analyzes and makes connections between empirical studies to define or advance a theoretical position, a theory explains why or how

evolution

descent with genetic modification, change in characteristics of living things over generations— as organizations pass on traits over generations, genes change in organisms overtime

• populations of organisms undergo slow, gradual change in their heritable traits

• change depends on random mutations in genes and adaptations to different environments- some help, some hurt

• unpredictable, natural

speciation

two populations become different enough, causing them to no longer be able to interbreed, giving rise to new species

artificial selection

traits are selected by the breeder, not necessarily promoting survival

evidence for evolution

1. fossil record

2. biogeographical evidence

3. anatomical evidence

4. developmental evidence

5. biochemical evidence

6. genetic evidence

fossil record

by observing fossils found in sedimentary layers, we have discovered life that is not alive today

• deeper layers= older

• simple organisms appeared on earth first (single celled—> multicellular)

• complex traits appeared overtime

biogeographical evidence

distribution of living species on earth due to continental shift

• identical fossils of organisms are found on continents separated by ocean

• very similar species can be found living on continents separated by ocean

anatomical evidence

homologous structure- similarity in body structure that share a common origin likely due to similar ancestry

analogous structure- body structures that share similar function but very different origins, its possible to evolve similar strategies as adaptations to similar environments

vestigial structure- body structures that no longer function but are similar to structures in other organisms

Developmental evidence

• humans have 3 cell layers- endoderm, mesoderm, ectoderm and so do other animals

• vertebrate embryos are very similar early on in development

biochemical evidence

more difference in genetics= more time from common ancestor

• similarities in DNA, RNA, genetic code

more similar looking organism have more similar genes/DNA

family tree

shows how all species are related

evolutionary forces

factors that change allele frequency and introduce/create new alleles or get rid of them

mutation

the source of new alleles, all new alleles are due to mutations

genetic drift

bottle neck affect- by chance, alleles in a population are removed/die creating less genetic variation

Founder effect- individuals create a new population in an area and have less genetic variability in the new place than their place of origin

gene flow

introducing new alleles to a population increasing genetic variability

natural selection

environment influences the frequency of alleles in a population

1. physical traits vary in each generation

2. heritable traits can be passed on to offspring that are harmful, neutral, or beneficial to survival/reproductive success

3. mutation creates random variation

non random mating

life depends on the ability to survive and reproduce. We choose who we want to mate with (sexual selection)

pathogens

variety of forms- bacteria, viruses, fungi, worms

vary in transmissibility and virulence

bacteria

single-celled prokaryotic cells found everywhere on earth

• most are harmless and beneficial

• some produce toxins but can be treated with antibiotics

virus

use transcription and translation machinery of host cell to replicate

capsid- protein shell of virus

viral genome- DNA or RNA

first line defenses

protection barriers at points of entry- tears, skin, saliva, respiratory system, stomach, bladder

• microbiome- barrier on all surfaces to keep things from getting in the body

if pathogens make it past first line defenses, the body must seek them out and get rid of them

innate immunity

fast-acting and responds similar in strength to every pathogen for every exposure

• phagocytes

• non-phagocytes

• protective proteins

• physiological responses

phagocytes

engulf, digest, and expel pathogens (pac-man)

• neutrophils, microphages, eosinophils

Natural killer cells (non-phagocytic cell)

Secrete enzymes to destroy target cell membrane and then kill virus infected/tumor cells by cell-to cell contact

basophil (non-phagocytic cell)

WBC that releases histamine to stimulate inflammatory response. They also relsease heparin to prevent blood clotting so fluids and immune cells (WBC) can leak into damaged tissue

complement proteins

circulate blood in inactive state until they cross a pathogen, bind to surface of pathogen and make it a target for phagocytes

• promote inflammation and cell lysis (make holes in pathogen membrane to break down cell)

interferon proteins

released by virus infected cells

• bind to receptors on non-infected cell

  • causes them to prepare for viral attack

  • they make proteins that interfere with viral proteins to stop the virus

inflammation

innate response- warmth, redness, swelling, pain

1. damaged cells and mast cells in the area release histamine that causes capillaries become leaky and dialate to increase blood/fluid flow to the site which creates inflammation

2. compliment proteins from plasma diffuse out of leaky capillaries, marking bacteria to be killed

3. phagocytes squeeze through capillary walls to attack debris

cytokines

signal hypothalamus to initiate sick feeling

• sleep: more energy to fight infection

• decrease hunger- slow metabolism to stave pathogens

• reduce thirst- dehydration reduces transmission

• fever- higher temp decreases pathogens ability to survive

adaptive immunity

slow acting, cells look for specific antigens on the pathogen and has the ability to remember pathogens for a stronger and faster response to future exposures. Protect entire body, not just infection site

• antibody mediated immunity- B-Cells

• cell mediated immunity- T-Cells

antigen

proteins and carbs on the surface of pathogen that flag it

antibodies

proteins released by B-cell that bind to specific antigens

• many arrangements that can be made by rearranging genes

antibody-mediated immunity

1. B cell with matching antigen receptor/antigen binds to bacteria

2. The newly activated B-cell multiplies rapidly (clonal response)

3. Activated B Cell clones become plasma B cells or memory B cells

   • plasma B-cells- produce and release antibodies to fight pathogens

   • memory B-cells- promote faster recognition and response to returning pathogens

4. antibodies from plasma B-cells bind to antigens on pathogens

   • antibodies cause pathogens to clump together to prevent them from multiplying

   • other antibodies signal WBCs to phagocytize pathogens

cell mediated immune system

directly attacks pathogens and infected host cells

cell-mediated immunity

1. Antigen-presenting cell (APC) is created by engulfing a pathogen and placing antigens on it’s membrane

2. APC’s present antigens to T-cells

   • T cells are activated against all pathogens that contain the same antigen

3. Activated T-cells rapidly clone themselves to become memory T-cells that help with future immunity and cytotoxic t-cells that attack matching pathogens kill them by puncturing their membrane

perfornin

protein released by cytotoxic T-cells that creates hold in the membrane to kill it

granzymes

enzymes expressed by cytotoxic t-cells and natural killer cells that enter through holds created in membrane and trigger apoptosis

vaccine

antigens of a specific pathogen are delivered to the body to induce immunity without causing the disease

• B cells and T cells respons as if body is threatened

• memory B and memory T cells are created and stored

• created a stronger and faster future response to pathogens

antibiotics

substacned that kill or stop growth of bacteria to help eliminate the infection