Example Proposal Title: Taller wheat plants by disconnecting gibberellin signal
ID: 187714 • Letter: E
Question
Example Proposal Title: Taller wheat plants by disconnecting gibberellin signal transduction. Objective: The objective is to determine whether cell expansion is limited by amounts of the hormone, gibberellin Hypotheses: (1) If the transcription factor (Txn), normally bound to the gibberellin receptor, is mutated so that it cannot bind the receptor, then Txn will continuously turn 'on' the expression of genes encoding proteins for cell expansion (see Fig 1) even in the absence of GA. (2) If GA does limit cell expansion, then the mutant plant will grow taller than the normal wild-type plant. Background: Gibberellin is a hormone that stimulates cells in stem internodes to expand. The extent of cell expansion influences the final height of the stem. The cells of the internodes are not continuously exposed to gibberellin. The amount of gibberellin varies in response to environmental conditions, and time of day as a function of the plant's circadian rhythms. No Mutaat Ga Gibberellin (GA) stimulates cell expansion by binding to a protein receptor. Binding causes the receptor to change shape and release a transcription factor (Txn), which then turns 'on' the expression of numerous genes encoding proteins that coordinate cell expansion. When GA is not present, then Txn is bound to the receptor and cells do not expand, so limited amounts of GA may result in limited cell expansion turned. on taed on We propose to mutate Txn so that it can not bind to Figure 1: In normal wheat plants, genes encoding proteins that direct cell expansion are the GA-receptor. We expect that the mutant Txn will turn 'on' not expressed until after gibberellin (GA) binds gene expression even when GA is not present. If so, then cell expansion should continue regardless of environmental factor (Txn). A mutant Txn that does not bind conditions and circadian rhythms, and result in taller wheat to the GA rece plants to its receptor, which releases a transcription ptor, turns on gene expression even in the absence of GAExplanation / Answer
TITLE: Poison Dart Frog resistant to Neurotoxin and its other purpose
OBJECTIVE: To find out what advantage does the point mutation give to this poison dart frog and what is the advantage of stuidying point mutation in sodium channels
HYPOTHESIS:1) Poison Dart Frog called Phyllobates terribilis, contains batrachotixin(BTX), on its skin to kill 20,000 mice and 15 growing men,normally this disrupts nerve activity by jamming open sodium channels and cause death,of itself this happens when there is no mutation
2) But when there is point mutation within single aminoacid in its own version of sodium channel protein, the frog is protected against this toxin, by altering sodium gated channels.
BACKGROUND: Point mutation is change of base sequence in codon, BTX acts as defensive mechanism against predators, BTX receptor has been delineated along the Na+ channel inner cavity, which is jointly formed by four S6 transmembrane segments from D1 to D4 domian, there were five aminoacid substitution mutation studied and it was found that changing aspargine residue to threonine conferred resistant to the poison without altering the gating properties of sodium channel this was by changing single base pair the coding DNA Sequence.
so by studying gene mutations in proteins of sodium channels, it is easy to identify advance targeted drug therapy, as because mutation in proteins of sodium channels can result in variety of disease, and BTX which blocks sodium channels can be used as sodium channel blockers, sodium channel blockers are used for treatment of epilepsy syndrome.
SIGNIFICANCE: Sodium channel protein mutations can be used to study advanced target drug therapy for variety of disease.
BTX blocks sodium channels which can be used as sodium channel blockers, mainly used in treatment of epilepsy syndrome
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