You really are a bore. Changes in the Hox genes have been shown to result in unfavorable mutations. The famous case is the one in the flies where a change in the Hox genes destroyed the stabilizers of a fly and replaced them with wings. This made the fly less able to fly. The scientists won a Nobel Prize for it. Here is the previous discussion about us on the matter:
The only thing the mutation did was destroy the production of some of the legs of the insect- in the same way that drug use by the mother destroys the brains of their children. In addition, turning off genes is not creating a more complex organism - as evolution requires - it is destroying complexity. If you were trying to prove that bacteria devolved from humans, you might have a point, but you are trying to prove the opposite. That you (and evo 'scientists') claim that a destructive mutation is a proof of evolution shows quite well the utter desperation of evolutionists in trying to prove their theory.
Further, you and your evolutionists continue to ignore the challenge which I posed. All I am asking for is a concrete example, a real example of a single species which has transformed itself from a simpler species to a more complex one. If evolution were true there should be numerous examples of such transformations amongst the millions of species living and dead. Numerous examples should have been found in the 150 years in which evolution has been claiming that it is true. Just one example showing "Macro-evolution is a transformation requiring new genes, more complexity and new faculties. In terms of genetics, it requires at a minimum the creation of more than one new gene. In terms of taxonomy it would require an organism to change into a different genus."
The problem is not that a mutation can destroy something - such as the legs of insects as this study shows. We all know that mutations can destroy things and that is one of the strongest arguments against evolution. Mutations in the developmental program, such as from women who take drugs can destroy the brains of babies also, I guess you wall that a proof of evolution also?????? Here's your link again so that all can see this mutation deletes information, it does not add anything to the organism.
Here is the proof that the developmental process of an organism is a program:
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.
Those changes I referenced were NOT destructive. The mutation in Ubx bestowed the ability for it to become a transcriptional repressor. Other mutations just led to different morphologies. Don't blame your illiteracy on evolution.
Note how complicated it is. Note that these scientists call it a program. Note that small changes or mistakes lead to disastrous results.
And as has been stated a hundred times, your interpretation is largely incorrect. Genes can be added or knocked out of mice with usually no ill effects.