Why? More clotting factors, more growth factors, more immunogenic factors are three examples I can think of off the top of my head which at some point were shown to have beneficial additive effects certain contexts.
First of all, you must realize that a gene is not 'on' all the time.
Many genes become constiuitively expressed once a stage in development has been reached. Besides, so what if the gene is not "on" all of the time anyway? If at the appropriate time, more of the gene product means a better chance for survival for the organism, who cares? Your rules are very arbitrary.
So leaving it on a little longer can do the job just as well almost all the time rather than having two identical genes
This is probably a bit trickier to produce than simply duplicating the sucker.
A gene to work has to get linked to the rest of the organism.
A duplicated gene will have all of the promoter elements necessary for its expression.
This is a big problem, perhaps the biggest problem for evolutionists and a problem which those 'fools' who preceded Darwin were well aware of but did not have the means of proving. Now the proof has been found.
??
A duplicated gene will have all of the promoter elements necessary for its expression.
This is just wishful thinking on your part and not fact. There is no reason at all why such a thing would happen in a random mutation. In addition you do not seem to fully understand the problem. Different functions require different kinds of cells. You need to have cells assigned to do the gene's work and to be of the proper constitution. A new gene, even a duplicate would not possibly have such a thing in the genome. In addition to which if it was just a xerox copy, it just would at most double the functioning of the old gene which is very likely to be harmful.
A duplicated gene will have all of the promoter elements necessary for its expression. - RWN -
This is a big problem, perhaps the biggest problem for evolutionists and a problem which those 'fools' who preceded Darwin were well aware of but did not have the means of proving. Now the proof has been found. -me-
?? -RWN-
We already spoke about how a gene is only the section which is transcribed to make proteins. What you are saying is just the latest excuse by evolutionists for scientific advances which disprove it.
Evolutionists have (and have always had) a very simple minded view of how an organism functions. This view is totally incorrect. It was incorrect in Darwin's time and it is even more incorrect now. One of the reasons I say that evolution has been disproven by science already is that the complexity guessed at before Darwin has received definite proof since then. Just note this: every single scientific discovery in biology has shown that the methods by which organisms operate and function are ever more complex. Mendelian Genetics discovered the dual nature of our genome. The discovery of DNA revealed how complex a gene was, how specific it needed to be to perform its functions, and how many of them there were. Now with the beginning of the unraveling of the genome, we are beginning to see how the deep interconnections between different parts of the body actually work. In other words, evolutionist reductionism has been totally destroyed.
I have spoken of how complex the 'program' by which life turns an organism from a single cell to a full grown one is, let me back up the above with the passage below:
23. Cell Interactions in Development
In Chapter 14, we learned that regionalization along the anteroposterior axis in the early Drosophila embryo is largely determined by gradients of transcription factors generated through translation of spatially restricted maternal mRNAs and subsequent diffusion of the encoded proteins through the common cytoplasm of the syncytial blastoderm. These transcription factors, in turn, control the patterned expression of specific target genes along the anterioposterior axis. In contrast, local interactions between cells, mediated by secreted or cell-surface signaling molecules, determine regionalization along the dorsoventral axis in Drosophila and along both major axes in early vertebrate embryos. Such local interactions also are the primary mechanism regulating the formation of internal organs such as the kidney, lung, and pancreas. Likewise, the vast number of highly specialized cells and their stereotyped arrangement in different tissues is a consequence of locally acting signals.
The importance of cellular interactions in development was demonstrated first in the early part of twentieth century through two complementary experiments. In one, destruction of an optic-vesicle primordium in developing frogs prevented formation of the lens from the overlying ectodermal cells. Conversely, transplantation of an optic-vesicle primordium to a region of ectoderm that normally does not give rise to a lens induced formation of a lens in an abnormal (ectopic) site (Figure 23-1). In modern biology we now use the term induction to refer to any mechanism whereby one cell population influences the development of neighboring cells.
In some cases, induction involves a binary choice. In the presence of a signal the cell is directed down one developmental pathway; in the absence of the signal, the cell assumes a different developmental fate or fails to develop at all. In other cases, signals can induce different responses in cells at different concentrations. For instance, a low concentration of an inductive signal causes a cell to assume fate A, but a higher concentration causes the cell to assume fate B. The concentration at which a signal induces a specific cellular response is called a threshold.
In many cases, an inductive signal induces an entire tissue containing multiple cell types. Two models have been proposed to account for these properties of extracellular signaling molecules. In the gradient model, a signaling molecule induces different fates at different threshold concentrations. A cell’s fate, then, is determined by its distance from the signal source. In the alternative relay model, a signal induces a cascade of induction in which cells close to the signal source are induced to assume specific fates; they, in turn, produce other inductive signals to pattern their neighbors.
Although inductive interactions often are unidirectional, they sometimes are reciprocal. Prominent examples of reciprocal induction include the formation of internal organs such as the kidney, pancreas, and lung. Many inductive interactions occur between non-equivalent cells; that is, the signaling and responding cells are already different. However, interactions between equivalent cells often are crucial in assuring that some cells in a developing tissue assume a specific fate and others do not. An evolutionarily conserved class of ligands and receptors regulates such interactions in C. elegans, Drosophila, and vertebrates.
Another feature that distinguishes various developmental pathways is the nature of the extracellular inductive signals. Many are freely diffusible and hence can act at a distance, whereas some are tethered to the cell surface and are available only to immediate neighboring cells. Still others are highly localized by their tight binding to the extracellular matrix. Early embryologists noted that cells differed in their ability to respond to inducing signals. Cells that can respond to such signals are referred to as competent. Competence may reflect the expression of receptors specific for a given signaling molecule, the ability of the receptors to activate specific intracellular signaling pathways, or the presence of the transcription factors necessary to stimulate expression of the genes required to implement the developmental program induced.
In this chapter, we first describe examples of various types of inductive signals and cellular interactions that regulate cell-type specification in several different developmental systems. Specific extracellular signals also control the migration of certain cells, which occurs during development of some tissues. As an example of this phenomenon, we discuss the role of extracellular signals in the assembly of connections between neurons. Another common feature of developmental programs is the highly regulated death of certain cells. In the final section of this chapter, we examine the conserved pathway leading to cell death and how it is controlled. The examples presented in this chapter were chosen to illustrate key concepts in this rapidly advancing field.
From: Cell Interations in Development
Note how complicated it is. Note that these scientists call it a program. Note that small changes or mistakes lead to disastrous results.