<p>so like the lac operon? and then the stuff with the enzyme/substrate stuff.
Is this right or am i just completely off?</p>
<p>That’s a good start. There is also alternative RNA splicing. I think there are other things besides this, but I don’t know them, so any help is appreciated. </p>
<p>And the enzyme substrate really isn’t something that controls the regulation from gene to protein.</p>
<p>^can you try to reword the question? I still dont know what your asking.</p>
<p>how prominent is anatomy on the bio test? i mean how important is it to know the functions of the nervous and circulatory systems, etc. we barely did that at all, if its important, i’ll cram it in this weekend</p>
<p>I would just memorize it, it doesn’t talk long. Maybe an hour, two ours max.</p>
<p>Many things, Senior0991. Dna methylation, deacetylation turns off genes. You need transcription factors and maybe activators to start transcription. mRNA is degraded in the cytoplasm after a certain amount of time.</p>
<p>Ok thanks!</p>
<p>Um i guess ill give another question.
What is the order of photosynthesis?</p>
<p>darkflame</p>
<p>ok thanks, because you guys are mentioning a lot of things in here i don’t know related to hormones and anatomy lol, i know plants, and molecular stuff (respiration, photosynthesis, dna/rna/protein synthesis) pretty well, as well as fungi and protists, is anatomy all i should focus on or am i missing anything?</p>
<p>oh and i’ll contribute to the thread, lol</p>
<p>describe the process of protein synthesis from start to finish</p>
<p>^ Lol, long process there.</p>
<p>Thanks Keasbey, I know my processes fairly well, but I always have a problem with remembering vocab, which is pretty significant in the FRQ. I will know what a vocab word means when I see it, though.</p>
<p>light reaction-
Starts with water spliting, releasing oxygen, and giving the electrons to PII (aka P630) Once electrons bottle up in cholophyll A the electrons are passed to the electron acceptors(they are excited) and the electrons pass thought the electron trasport chain. (H+ is pumped into the chylorplast) and finally the electrons reach another electron acceptor. The electrons are than passed to PI (aka P700) and once again they are excited and passed to another electron acceptor. From here the electron moves to NADP+ sythase and NADP+ + electrons + H = NADPH. (this is known as cyclic phosporlation)</p>
<p>Electrons can also move from PI back to PII so electrons can move thougt the electron trasport chain again and pump more H+ into the choloplast. The H+ goes into ATP syntase and creats ATP (adenine triphosphate?) ADP + H+ = ATP.</p>
<p>gonna fresh up on Dark reaction (kalvin cycle)</p>
<p>thanks marcus</p>
<p>First, water is split, which releases two electrons. The electrons go to Photosystem II, and are excited from the reaction center by light energy. They then travel down an electron transport cascade, which transports hydrogen into the thylakoid space. The electrons then hit Photosystem I, where they are re-energized, and this time they are eventually accepted with a proton by NADP+ to form NADPH. The proton gradient fuels ATP production through ATP synthase. Because cells need more ATP in the next step, they use cyclic photophsophorylation, which uses only photosystem I to only produces ATP (because the electrons are cycled and thus not accepted by NADP+). </p>
<p>The NADPH and ATP then are used to tranform 3 CO2 into one glyceraldehyde-3-phosphate. The 3 CO2–one carbon atom–complex with three Ribose 1,5 biphosphate–each has 5 carbon atoms–(with help from rubsico) to form three short lived intermediates–each with six carbon atoms–which quickly form six 3-phosphoglycerate–each has 3 carbon atoms. ATP and NADH are used to transform this into 6 molecules of glyceraldehyde three phosphate, one of which is released to be used in saccharide production, and the other 5 G3Ps use ATP to reform the three Ribose 1,5 biphosphate.</p>
<p>The first paragraph are called light-dependent reactions, the second is light-independent reactions, also known as Calvin cycle or dark reactions.</p>
<p>Before we start talking about how protein is made you know have to know about three different RNA. First mRNA (messanger RNA) copies DNA and transports it into the nucleus. Second tRNA which translates the mRNA, and is shaped as a clover. Amino acid is attached to the 3’ end, and anticodons are attached to it. and rRNA, ribosomes that help in translating the mRNA. There are two subunits (S40, S60, total of S80) </p>
<p>RNA primase come in and lays down the ‘road’ for polymerase to create the mRNA. ( which polymerase?) The polymerase than attaches the codon matching the DNA. (A with U, T with A, G to C, and C to G) after that mRNA is altered. small nucleic ribosomes proteins? cut up the interons and leave the exons (expressed gene) the exons rearrange to make new mRNA sequences which will make different proteins. A guanine cap is added on the three end and poly A tail on the five end. Next the mRNA goes into he cytoplasm.</p>
<p>When in the cytoplasm the mRNA binds to a rRNA subunit (S40). tRNA with met amino acid comes and binds to the P (polypepitde) space. next the S60 rRNA binds. After that another tRNA comes and attaches to the A (amino acid) space. The P tRNA gives its amino acid to the A tRNA, and the A tRNA moves to the P location. THis keeps repeating until the stop codon is reached. After this a release factor attaches to the A space, and the amino acid sequence is released. The amino acid than forms various bonds (beta plated and alpha helix) which bond with other amino acids to form a tertiary structure. Multiple tertiary structure bind to produce a quantinary structure. The bonds used in tertiary and quaninary are ionic, hydrogen, disulphide, and covalent bonds. The protein may not be active until it recieves a single or a piece of the amino acid sequence is removed. </p>
<p>sorry for the spelling mistakes (im tired) can someone please check it? </p>
<p>Nite everyone dont let this thread die!!!</p>
<p>wow, this thread is intense.</p>
<p>@darkflame:good job, the only thing I would add is that I think the name of the protein that splices the introns off from the exons is called a snurp(sp?). and I don’t know how important it is, but I would separate the processes of sythesizing a protein from initiation, elongation, and termination.</p>
<p>SNRPs (prounced snurps…i believe it stands for single nuclear ribonucleac proteins, although i’m not 100% on that)…they associate with other proteins to form a spliceosome and carry out the splicing of the introns and exons</p>
<p>To clarify: Small Nuclear Ribonucleoproteins, also known as snRNP or “snurps” form with some pre-mRNA to form spliceosomes, which are the protein-complexes that splice introns from the RNA.</p>
<p>I believe sNRPs recognize the splice sites and cuts the introns out and join the exons.</p>
<p>
I totally agree…</p>
<p>oh, okay thank you. So I would guess that the spliceosome is more important to know than the snrps?</p>
<p>adding to the thread, I have a test on this tomorrow: outline the different processes of humoral response and the cell-mediated response of the immune system.</p>
<p>I don’t know much about immune system, but here we go: The membranes of cells have MHC markers that distinguish between self and foreign cells. T-cells are activated, increase in number in response to foreign cells. Helper T-cells activates B-cells and other T-cells. Memory T-cells, well, stores the memory of pathogen and response quicker in the future. Cytotoxic T-cells kills the pathogens. T-cells and B-cells are formed in bone marrow, but T-cell is matured in thymus (t for thymus).</p>
<p>What is cyclin, Cdks, MPF? How do these control/influence the cell cycle?</p>
<p>MPF is also known as Mitosis promoting factor which is also known as a M cyclin-CDK kinase or M-CDK. Basically, it is a complex of a cyclin, and a cyclin dependent kinase or CDK (kinases, if you recall, transfer phosphate groups and thus activate other proteins). The CDK requires cyclin to bind with it to work. For MCDK, M cyclin is needed to bind to the particular CDK that forms MCDK. The concentrations of cyclin vary throughout the cell cycle, while the concentrations of CDK remain the same. Before mitosis starts (during G2 phase), the concentration of M cyclin increases exponentially (I don’t remember exactly why, but I think it has to do with the degradation of SCDK, which promotes DNA synthesis), so thus a large amount of MCDK is formed. This MCDK is inactivated by a phosphate group in the wrong place until the cell is completely ready to enter mitosis. Once the inhibitory phosphate is removed, MCDK is activated, and it does such activities as breaking down the nuclear lamina, causing formation of the spindle microtubules, condensing chromosomes, etc. The APC, or anaphase promoting complex (which, predictably causes anaphase) leads to the breakdown of M cyclin through ubiquination, thus inactivating MCDK as a result, to allow all the processes caused by MCDK to reverse. </p>
<p>My explanation may have some flaws. If you have any further questions, feel free to ask. This is a very complex subject, and I can probably provide you with a better answer if I consult some other sources. </p>
<p>You don’t need to really know much about the above explanation for the AP Test, as it is advanced college cell biology. You should know some of it, though, like how the M cyclin concentration changes throughout the cell cycle.</p>
<p>That is correct Senior. Also the amount of cyclin will alter which stage the cell is in and will control the speed of the cell cycle. In cases where the cell cycle is unregulated (cancer) there would be a problem, such as cyclin concentration does not decrease. This will keep the cell continually dividing into a tumor.</p>