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Berkeley MCELLBI 140 - CLINE 11

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PowerPoint PresentationSlide 2Slide 3Slide 4Slide 5Slide 6Slide 7Slide 8Slide 9Slide 10Slide 11Slide 12Slide 13Slide 14Slide 15Slide 16Slide 17Slide 18Slide 19Reading:pp152-154 Mitotic recombination can produce genetic mosaics (-- and cause cancer)I’ve asked to reserve a lecture room from 7-9pm Thursday,April 5, for a review session in connection withthe midterm on Monday, April 9. I’ll announce where the sessionwill be held as soon as I know myself.(1) genetically sensitize the system: “turn” lof recessives into dominants (but only with respect to one non-essential aspect of their function)Poising the activity level of “your favorite gene”on a phenotypic threshold to make other genes haploinsufficient…but only with respect to the functioning of “your favorite gene.”Last Friday:So that: (1) we can identify new mutations of interest in the F1 generation(first generation after mutagenizing the parents)AND(2) can overcome some complications of pleiotropy …so that we can more easily study the non-vital aspects of thefunctioning of genes that ALSO have vital functions(1) genetically sensitize the system: “turn” lof recessives into dominants (but only with respect to one non-essential aspect of their function)…if take away that cushion for any one gene in a pathway,now make the normal operation of the pathway…with respect to that one gene…more vulnerableto reductions in other gene levelsWildtype fly must normally have an excess of most genes’ activityas insurance against fluctuations in the levels of activity of various genes in a pathway during developmentBased on the rationale that:(2) use targetted genetic mosaics to screen for recessives in the F1 (homozygous clones in heterozygotes …in non-essential tissues only!)…recover new recessives in the F1???(without making them dominant?)Another way around the limitations of pleiotropy in genetic screens:genetic mosaicsgenetic mosaicsaccording to your text: “an organism containing tissues of different genotypes”genetic mosaicvs: (genetic) chimera:cells an embryo or animal composed of cellsfrom two or more different organisms…all derived from a single initial cell (zygote)individualsorganism(and that’s what they say in the text)genetic mosaics are extremely useful for determiningwhere a particular gene’s function is needed:Fig 20.4:+++--+Your text short-changes the key concept of cell autonomy in gene functiongenetic mosaics are extremely useful for determiningwhere a particular gene’s function is needed:L1L2L1L2non-mosaicag- mutantphenotypiceffect ofag- vs. ag+In what cell type (L2 vs. L1) is ag+ function neededto elicit normal differentiation of L1?genetic mosaics?L1L2L1L2non-mosaicwildtypedifferentiationL1 differentiatesnormally despitebeing ag-L1 differentiatesabnormally despitebeing ag+L1L2L1L2ag-ag+For ag, the cell whose phenotype is mutant is not the cell whose genotypeis mutant. Hence ag is not cell autonomous with respect to the L1 phenotypemosaicL1L2L1L2ag-ag+mosaicL1L2L1L2non-mosaicag- mutantL1L2L1L2non-mosaicwildtypewhitemarks ag-The “genetic marker” is cell autonomous ,since the cell whose marker phenotype is mutant is the cell whose marker genotype is mutant.…if a cell’s genotype in the mosaic dictates that cell’s phenotypeag seems to work in L2 to signal L1 (like boss)Where isag+ needed?(that’s why it was chosen)…ag is non-autonomous with respect to the L1 differentiation phenotype When discussing autonomy/nonautonomy, need to specify the phenotype in question:L1L2L1L2ag-ag+L1L2L1L2ag-ag+L1L2L1L2non-mosaicag- mutantL1L2L1L2non-mosaicwildtypeag seems to work in L2 to signal L1ag-ag+…perhaps ag is autonomous with respect to generating the signal in L2.(if we had an assay for the signal, we might see that phenotype directly)ag isnonautonomousFig. 14.33first nucleardivision of azygotedo males normallyhave white eyes?XXw-/w+XOw-/--T.H.Morgan published on genetic mosaics in 1914: Hence,~50%w+ vs. w-…too largeforour purposesXOXXotherwisediploid(AA)(2) use genetic mosaics to screen for recessives in the F1 …look for homozygous mutant clones in otherwise heterozygous animals …identify (and recover) new recessives in the F1Another way around the limitations of pleiotropy in genetic screens:provided -- one generates clones in only a small fraction of all cellsor-- one generates clones only in non-essential tissueseven works for new mutants that are recessive lethal or sterileBased on a phenominon discovered (‘30s) by former chairof U.C. Zoology Dept: mitotic recombination…only possible because of a very strange aspect offly chromosome behavior:homologous chromosomes pair during mitotic interphasebut improved upon enormously in modern timesAnother way around the limitations of pleiotropy in genetic screens:(2) use genetic mosaics to screen for recessives in the F1 …look for homozygous mutant clones in otherwise heterozygous animalsStern’s observation:…for fly heterozygous for recessivecell-autonomous l.o.f. allelesof two genes:yellow(body)- singed(bristles)+yellow(body)+ singed(bristles)-most flieswildtypeIf irradiated (ionizing) during developmentoccasionally sawodd ADULT fly:patch ofy/y ?patch ofsn/sn ?“twin spot”deduced:mistake in mitosis,not new mutant allelesFig. 5.23 p152Consider what it is about mitosis that insures daughtercells will have the same genotype as their mother cell:XmXpmpy+y-sn+sn-mmppy-sn+sn-y-sn+y+y+sn-if instead:pmpmy-y-sn+sn+y+y+sn-sn-mmy-y-sn+sn+py+sn-py+sn-then:mmppy-y-sn+sn+y+y+sn-sn-=What if DNA breaks and improper repair after S phasechange relationship between genes and centromeres:mpy+y-sn+sn-mmppy-sn+sn-y-sn+y+y+sn-NO CHANGE if instead:mistakey-sn+y-sn+y+y+sn-sn-mmppmmpppmpmy-sn+y+y+sn-sn-y-sn+yellowsingedtwin-spotDNA breaks and improper repair after S phasegenerate the “twin-spot” of cells homozygous for y and snmpy+y-sn+sn-mmppy-sn+sn-y-sn+y+y+sn-mistakey-sn+y-sn+y+y+sn-sn-mmppmmpppmpmy-sn+y+y+sn-sn-y-sn+twin-spot: because progenyof the y/y & sn/sn originalcells tend to stay togetherpatch (clone) ofy/y (yellow)patch (clone) ofsn/sn (singed)size of patches depends on whenabberrant mitosis occursADULTEXTERIORGrowthFig. 5.24 (p152)mpy+y-sn+sn-What if we had induced a NEW recessive MUTATION on a mutagenizedy- sn+ chromosome (in the father’s sperm) that affected cell growth


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Berkeley MCELLBI 140 - CLINE 11

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