Gedächtnisprotokoll WS18-19

A)

morphogen gradient

lateral inhibition

induction (cascades)

oscillating systems

reaction diffusion system

B)

a morphogen gradient can grow / expand proportional to tissue size —> scale it might need adjustment in stability, diffusion and transport rate

C)

an inhibitor can shape the gradient through a reverse gradient (sog inhib dpp)

A)

mutation in regulatory sequences

genetic alterations like transposons that hyperactivate the gene transkription

alterations of the chromosome, recombinational errors

alternative splicing

—> errors in DNA repair mechanisms

viral oncogenes (slowly transforming type)

B)

The Rb is part of the cell cycle control mechanism, in its active state it prevents the cell to enter S-phase by inhibiting the cyclin dependent kinases (CDK), specificly it binds the E2F transcription factor

It functions as a tumor suppressor so in tumorigenesis a loss of function is needed for the cancer to grow, that can be the destruction of the Rb protein or inactivation by phosphorylation or binding to a inhibitor molecule

inheritable mutations

homozygous mutation needed (like many TSG recessive manner)

C)

a shortened chromosome (22 q-) that by recombinational error lost (transferred) too many parts to the chromosome 9, through this error the genes of Bcr and Abl are in close proximity and translate to a tyrosine kinase that is hyperactive and promotes tumor characteristics

inhibition of the kinase by Imitinib (Gleevec) by blocking the active centre —> targeted therapie

Tumor addiction to that pathway

A)

it forms from the intermediate mesoderm

B)

the receptor Ret and the signal molecule GDNF are key for the formation of the uretric bud a gene mutation that cause the loss of one of them would result in no uretric bud, of course many signals are needed for this formation

—> GDNF mutation = no bud or Pax2 mutation

Ret receptor gain of function can result in multiple uretric buds or mutation in Foxc1/c2

C)

The kidneys are formed from the intermediate mesoderm the metanephrons give rise to the kidneys in the adult, it goes hand in hand with the gonads formation and starts with formation of the uretric buds through GDNF and Ret receptor signaling GDNF and WNT signaliing then control the branching mechanism of the kidney they are also responsible for the proliferation, growth and matureation of the kidney

• Wnt signals essential for nephron formation & branching morphogenesis of collecting ducts ( WNT11 tip positive feedback loop GDNF & RET, WNT9b acts on underlying mesenchyme -> mesenchym condensation -> WNT9b (stalk) -> ß-Catenin-> FGF8 -> WNT4. 3 Progenitor pools exposure to different concentrations of WNT9b in the stalk -> differentiation -> fusion with duct -> Nephron patterning with Glomerulus

A)

wenn mit Aminosäuren die basenpaarung gemeint ist dann complementary base can pair and form 3D conformational structures because the nucleinbases Adenin, Uracil, Cytosin and Guanin interact, besides that only the sugars (Ribose) have interaction potential

B)

Pseudoknots develope by the interaction between the bases (single stranded loop with double stranded region in RNA) they bind and intertwine by that they are different to the hairpin structures

often found in complex RNA molecule structures like tRNA or rRNA

C)

the initiator tRNA with Methionin as the AA to the start codon AUG

mutible initiation factors eIF2 , eIF3 (prevent binding of large ribo subunit until AUG is there), eIF4E (know from 4E-BP which is inhibited through phosphorylation by mTORC1) that help

5´cap structure as a recognition (eIF4E binds there) and protection signal

A)

collagen IV

laminin, nidogen, perlecan

integrin (transmembrane to cells)

collagen VII connection to dermis

B)

by EMT through which the adhesive structures of the cell downregulate

by Matrix metallo proteases that cleave adhesive structures, a way through the basal membrane and activate further MMPs by cleavage until the way into the blood stream is clear (—> local invasion and intravestation)

C)

Important to achive the key factor to gain invasiveness is motility, the tumor cells can disseminate and metasthasize in the organism through EMT which is a developemental or wound healing (regeneration) programm of the organism then surrounding cells and especially the protesesare “tricked” into helping the cancer cells reach invasiveness

D)

Gain of mesenchymal properties

Wound healing , regeneration , embryonic developement

TGF-ß

SNAIL transcription factors

TWIST

SLUG

Inflammatory cytokines