1. Armadillo promote naked curticle posterior non-hair fate downstream of wingless,right? yes! Armadillo mutant, however, make posterior cell of fly into hairy, right?Did I understood correctly? yes, in an armadillo loss of function mutant, all the cells inthe segment would develop hairs2) Is X-chromosome modification because of H19 methylation (base changemodification) or acetylation (non base change modification) or both? I think you mayhave a typo here--H19 is an imprinted gene, it doesn’t have anything to do with X-chromosome inactivation. The acetylation status of histones, methylation of histones(both non base change modifications since it affects the histones not the DNA itself)AND methylation of DNA (base change modifications) have important roles in X-chromosome inactivation—the details are covered in your reading.3) In lecture 6, when you were discussing imprinting, you said that there were 70 genes inmammals only on the sperm or egg allele that are active, but in the book it says 75?Good eye, it sounds like a few more imprinted genes have been identified, so I would gowith 75! This is not something I would have taken points off for in an exam situation.4) When Ubx is expressed in T3 and A1, how does it affect A1 differently than T3 orshould we just know that they turn on specific genes? Ubx activity should preventexpression of genes active in the T2 (and more anterior segments) from expressed in theT3 and A1. we would predict that since different genes would be activated in T3 vs. A1,the presence of other homeotic genes would influence the difference between these twotypes of segments.5) what do you mean by the abdominal A and B segment regulation? are you justisolating certain parts? not sure exactly what you mean here. abdominal A andabdominal B are two other homeodomain proteins that affect the identify of theabdominal segments. We talked about how if you have fly embros that have mutations inUbx, AbdA and AbdB, you get a T2 fate spreading throughout the T3 and all theabdominal segments. This implies that AbdA and AbdB are preventing T2 fate in A2 andon, and Ubx is preventing T2 fate in T3 and A1.6) could you clarify the second to last slide discussing the notch and delta cellular roles?Delta is a membrane-bound signal that is active in cells that have ingressed from the layerof epidermal cells and will become neuronal. It interacts with the Notch transmembranereceptor expressed in the cells remaining behind in that epidermal layer. Activation ofthe Notch signaling pathway in those epidermal cells keeps them from ingressing andtaking on a neural fate. We also talked about how the intracellular part of the Notchprotein is cleaved when it is activated, and it moves into the nucleus where it interactswith other proteins to regulate gene expression.7) when you talked about retroviruses causing cancer by activating proto-oncogenes doyou just mean that when there is a Wnt-1 mutation it will cover the engrailed sequenceand lead to this cancer? not exactly. the insertion of retroviruses in a chromosome canaffect when a nearby gene is expressed. Misexpression of some genes is known to causecancer. It was found that inappropriate expression of Wnt-1 and activation of the Wntsignaling pathway can lead to tumor formation. Since we know that engrailed expressionis kept on by Wnt activity (we talked about this in the context of segment polarty and inthe brain), you could predict that it might also be affected by misexpression of Wnt, butthe retrovirus insertion itself wouldn’t be anywhere near the engrailed gene.8) from the final lecture, number 10, could you clarify between which factors are trans vs.MAD, and exactly what a MAD factor is? I couldn't find enough information in the book.All the proteins we talked about that regulate floral meristem identity or floral organidentity are transcription factors, they all regulate the mRNA expression of other genes.A MADS-domain protein is a type of transcription factor, just like a homeodomainprotein is another type. Classes of transcription factors are frequently named after thepart of the protein that binds DNA, ie. the MADS-domain. AP1, CAL, AP3, PI and AGare all MADS-domain transcription factors, LEAFY and APETALA2 are two differenttypes of transcription factors.9) how does the trans representation of Apetala 2 prevent the activation of the center of aflower? I think you are asking why wouldn’t expression of APETALA2 throughout thefloral meristem prevent the expression of AGAMOUS in the center of the flower?Unlike the other transcription factors we talked about, the activity of APETALA2 is notcontrolled at the level of transcription. It regulated by translational repression instead.Therefore, even though the AP2 mRNA is present throughout the flower meristem, theAP2 protein is not produced in the center of the flower meristem, so it doesn’t affectexpression of AG. Like APETALA1, AP2 activity in the first two whorls would repressexpression of AG.10) how doe you know that Agamous is sufficient to specify identity, but the LOF mutantsays it is necessary for identity? The terms ‘necessary’ and ‘sufficient’ are two differentterms that are frequently used to describe what is known about genes involved indevelopment. A gene like AG is necessary for development of the stamens and carpels,and to make the floral meristem determinate. The agamous loss-of-function mutantdemonstrates this. It turns out that the GOF experiment we talked about, where theAGAMOUS gene was hooked up to a promoter that would direct its expression in thepart of the floral meristem that would become the sepals, showed that AG is alsosufficient to specify a carpel fate in these cells that would normally have a different fate.11) Could you reexplain the cell-type selection, division asymmetry, and mother-daughter difference type of cell lineage mutant. This last case is where the daughter cellwould typically have a different fate/different lineage pattern than its mother in awildtype worm, but instead the daughter cell repeats the fate/lineage pattern of its motherin a mutant worm. You can sometimes see successive generations of cells get stuck in aparticular pattern, which was the example shown on the ppt slide. Division asymmetrymutants are when two daughter cells would normally have different fates, instead havethe same fates in a mutant. A cell type selection mutant, would be if a daughter cellwould normally
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