Answer:
true
Explanation:
cuz it's true also trust me I've done my research.
A population with a lot of genetic variation would likely have more phenotypic variation; therefore, such a population would more likely have individuals that can adapt to a changing environment. mutation can result in new alleles on chromosomes. ... this is the same effect that genetic drift can have on small populations.
Answer: <em>D. Causes an accumulation of lipids in brain cells</em>
Explanation:
Tay-Sachs disease is caused by a genetic mutation in the <em>HEXA</em> gene. It is an autosomal recessive disease that causes the mutation on an enzyme, which metabolizes <em>GM2 Ganglioside</em> in nerve cells, this leads to a build-up of the molecule in brain cells. At the moment there is no cure for the disease, only support treatment is available.
<span>The generally accepted parts of modern cell theory include: All known living things are made up of one or more cells. All living cells arise from pre-existing cells by division. The cell is the fundamental unit of structure and function in all living organisms. hope this helps but you should be more specific in the future</span>
Answer:
please mark as brainliest answer as it will also give you 3 points
Explanation:
Cyclin-dependent kinases (CDKs) are the families of protein kinases first discovered for their role in regulating the cell cycle. They are also involved in regulating transcription, mRNA processing, and the differentiation of nerve cells.[1] They are present in all known eukaryotes, and their regulatory function in the cell cycle has been evolutionarily conserved. In fact, yeast cells can proliferate normally when their CDK gene has been replaced with the homologous human gene.[1][2] CDKs are relatively small proteins, with molecular weights ranging from 34 to 40 kDa, and contain little more than the kinase domain.[1] By definition, a CDK binds a regulatory protein called a cyclin. Without cyclin, CDK has little kinase activity; only the cyclin-CDK complex is an active kinase but its activity can be typically further modulated by phosphorylation and other binding proteins, like p27. CDKs phosphorylate their substrates on serines and threonines, so they are serine-threonine kinases.[1] The consensus sequence for the phosphorylation site in the amino acid sequence of a CDK substrate is [S/T*]PX[K/R], where S/T* is the phosphorylated serine or threonine, P is proline, X is any amino acid, K is lysine, and R is arginine.[1]
