Answer:
Cystic fibrosis mutation is recessive to normal allele because only one functional or normal allele is enough to produce a functional protein. So, if mutation is present in one allele then also, a normal protein can be made from normal allele. The presence of normal protein prevents the expression of disease.
In addition, mutated allele only results in the loss of function of protein which can be compensated by the expression of normal allele. It does not add any toxic effect to the protein. Consequently, the disease is inherited in autosomal recessive fashion.
In contrast, Huntington mutation not only alters the structure of the functional protein but also adds toxicity to it. The altered protein is enable to interact with 100s of other proteins and inhibit or decrease their function. So, if only one allele is present then also, the mutated protein will be produced and it will result in the phenotype. Consequently, it is inherited as autosomal dominant fashion.
14C (carbon-14) can be used to date a 20,000 year old skeleton
Hey, there! The correct answer to this question will be D. Acris crepitans.
Answer:
They can have children together. If they are married or in a relationship they can do anything they want together including the want of children.
Explanation:
A neuromuscular junction (or myoneural junction) is a chemical synapse formed by the contact between a motor neuron and a muscle fiber.[1] It is at the neuromuscular junction that a motor neuron is able to transmit a signal to the muscle fiber, causing muscle contraction.
Muscles require innervation to function—and even just to maintain muscle tone, avoiding atrophy. Synaptic transmission at the neuromuscular junction begins when an action potential reaches the presynaptic terminal of a motor neuron, which activates voltage-dependent calcium channels to allow calcium ions to enter the neuron. Calcium ions bind to sensor proteins (synaptotagmin) on synaptic vesicles, triggering vesicle fusion with the cell membrane and subsequent neurotransmitter release from the motor neuron into the synaptic cleft. In vertebrates, motor neurons release acetylcholine (ACh), a small molecule neurotransmitter, which diffuses across the synaptic cleft and binds to nicotinic acetylcholine receptors (nAChRs) on the cell membrane of the muscle fiber, also known as the sarcolemma. nAChRs are ionotropic receptors, meaning they serve as ligand-gated ion channels. The binding of ACh to the receptor can depolarize the muscle fiber, causing a cascade that eventually results in muscle contraction.
Neuromuscular junction diseases can be of genetic and autoimmune origin. Genetic disorders, such as Duchenne muscular dystrophy, can arise from mutated structural proteins that comprise the neuromuscular junction, whereas autoimmune diseases, such as myasthenia gravis, occur when antibodies are produced against nicotinic acetylcholine receptors on the sarcolemma.
