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[經驗分享→] 轉載 蟒蛇基因

轉載 蟒蛇基因

Genetics
Learn basic genetics for reptilekeepers and breeders

By Vincent J. Lynch

It seems nearly every reptile species commonly kept and bred by hobbyistss these days has at least one genetic color or pattern morph. With some species, such as ball pythons, corn snakes and leopard gecko, the number of morphs is truly overwhelming. This popularity has increased the use of genetic terms, which describe how morphs are inherited and predict the outcomes of morph crosses. Unfortunately, the morph explosion also has introduced confusing and sometimes mysterious genetic jargon and math into the hobby. But the genetics of reptile color and pattern mutations don't have to be difficult. Some biology basics make them easy to understand.

Building a Foundation

Animals consist of hundreds of millions of cells. Within each cell is a special compartment called the nucleus, and it houses the cell's genes. The sum of those genes - and all DNA between them - is called the genome. Except for sperm and eggs, each animal cell has two complete copies of the genome. One is inherited from the mother, and the other comes from the father. In principle, each copy of the genome;s estimated 60,000 genes is exactly the same. In reality, however, some copies have small differences between them. These are called mutations.



Mutations arise during the production of reproductive cells. The genome is copied and packaged into sperm and eggs. This process is nearly perfect, but mistakes happen. Consider the photocopy of a picture. Imagine copying the photocopy and then copying that copy. Do this long enough, and you'll notice small imperfections slowly distort the original image. Luckily, evolution has devised an error-checking system. Like a good proofreader, it compares a newly copied genome to the original and corrects mistakes. Yet even this mechanism isn't perfect. Mistakes can happen in nearly 3 billion places, so a few errors will slip through. Each new sperm and egg contains a handful of mutations.

Most mutations occur in functionally unimportant regions of the genome. They make no contribution to the animal's health or appearance. However, gene mutations disrupt a gene's normal function. If the mutation occurs in a gene important for pigment production, pigment storage or pattern formation, a new morph is created. http://www.creepers.com.cn/forum/index.php?action=dlattach;topic=678.0;attach=4152;image



For example, albinism results from a mutation that inactivates a gene called tyrosinase, which is vital to black pigment formation. But not all mutations are deleterious. Some can actually benefit the organism. Consider antibiotic-resistant bacteria. Their resistance stems form a mutation that enables an enzyme to break down antibiotics. Bacteria with the mutation have a powerful advantage when exposed to antibiotics. They survive and reproduce - even if that is bad for us humans.

Fortunately, a single gene mutation rarely causes things to go horribly wrong. Remember, each gene has two copies. If one copy goes mutant ,the backup compensates and takes over. These are two forms of the gene, one normal and one mutant, and these alternative forms are called alleles. Some alleles are dominant to others, which means they can completely cancel the effects of another allele.

Consider the albino example again. In this case there are two alleles. The normal allele is dominant to the mutant allele. This means neither an animal with two normal alleles, nor an animal with one normal and on mutant copy exhibits the albino trait. Both animals look completely normal. Only an animal with two mutant alleles will be an albino.

Suppose a gene has only two alleles like our albino. This pair can be combined in four possible ways. Let's call the normal allele of the albino gene "A" and the mutant allele "a". Alleles can be combined as AA, Aa, aA and aa. These allele combinations are called genotypes. Both Aa and aA are essentially the same, so we can reduce the complexity a little and say there are three genotypes: AA, Aa and aa. homozygous animals have the same alleles, such as AA and aa. Heterozygous animals have mixed alleles, such as Aa.

Remember, the normal allele (A) is dominant to the mutant allele (a) in our albino example, so the three genotypes can have one of two appearances. These appearances are called phenotypes. Because the normal allele (A) can completely cancel the mutant allele (a), animals with AA or Aa look the same. Without a functioning copy of the gene, animals with aa will be albinos.



Crossing Animals

Being able to predict the outcome after crossing two morphs is valuable tool to have. Although this power is fundamental to modern biology, it was not possible before the late 19th century. The major breakthrough came from the careful work of Austrian monk and naturalist Gregor Mendel. Named the "father of genetics". Mendel cultivated pea plants with several variable traits, including flower color, seed color and seed shape. Keeping careful records of parent and offspring appearance from more than 28,00 crosses, and he was able to make generalization on inheritance and predict the outcome of crosses.

Mende;s work went virtually unnoticed for half a century. It was not until 1900 that Reginald Punnet "rediscovered" Mendel's contributions and put them to use. Although Punnet made many contributions to the field of genetics, he is know for developing the Punnet square, a tool used for predicting offspring's genotypes and phenotype when the genotype of the parents is known.

Using the albino animal example again, let's cross it with a normal animal. The albino parent's genotype can only be aa. Assume the genotype of the normal parent is AA. This means an albino can only make sperm or eggs with the genotype a, and the normal animal can only make reproductive cells with A genotype. if you breed the animals, the offspring inherit an a allele and A allele respectively. Carrying the genotype Aa, all offspring are heterozygous for albino.

This outcome is easy to predict, but outcomes become more complicated when two heterozygous animals, or "hets", are crossed. This is where the Punnet square becomes handy. Breeders can useit to determine the genotypes and phenotypes of offspring as well as predict the probability of producing them.

Breeding hets of our albino example yield three possible outcomes: AA, Aa and aa. This example is relatively simple, but crosses can be much more complicated. Consider producing a designer morph such as a snow. These animals are albino and anerythristic, which literally means without erythrin, a red pigment. "Anery" animals lack red color and are usually various shades of black, white and gray.

The initial cross produces normal-looking animals that carry an allele for both albino (a) and anery (r). In other words, their genotype is AaRr, and they are double heterozygotes.

Constructing a Punnet square for double het is similar to a single het (our albino example) except now we have four possible genotypes for sperm and eggs: AR, aR, Ar and ar. Instead of four cells and four possible outcomes for our Punnet square, we have 16 cells and 16 possible outcomes. Only one of the 16 is the snow.

Things get considerably more complicated when three genes are involved. Crossing a triple het has 64 possible genotypes, and only one exhibits the trait you're after. You probably get the picture.

More Complicated Crossings

In our albino example, the alleles were clearly dominant or recessive, but this is not always the case. Simple genetic traits (such as albinos and anerythristics) can be explained by dominant and recessive alleles. Complex traits cannot be explained so easily. Several kinds of complex traits exit, but only a few are important for reptile breeding, such as incomplete dominant, co-dominant and multi-genetic traits.

Sometimes the appearance of the heterozygote (Aa) is different from both homozygotes (AA and aa) and lies somewhere in between the appearance of the two homozygotes. In this case, neither allele is able to cancel the effects of the other, so their effects blend. This type of inheritance is called incomplete dominance. It occurs because a mutation change how one of these genes functions but does not completely destroy it. Each allele in the hetrozygot will contribute something to the phenotype.

A good example of incompletely dominant traits has shown up in corn snakes. These snakes have three alleles of the tyrosinase gene: A, a and u. The genes are responsible for making black pigment. AA individuals are normal, aa are albino, and uu are ultra hypo, which is a very extreme - nearly albino - form of hypomelanism.



The incompletely dominant trait appears when an albino (aa) is bred to an ultra hypo (uu). Because the alleles cannot cancel each other out, the offspring have a third phenotype that splits the difference between albino and ultra hypo. These "au" individuals have been called "ultra amel" or "ultramel" and have more dark pigment than an albino, but much less black pigment than a normal animal. Thus the alleles a and u are incompletely dominant to each other, yet both are recessive to A.

Unlike incompletely dominant traits, trait co-dominance is the special situation when both alleles are expressed at the same time, so the phenotype is a mixture - not a blending - of both homozygous phenotypes. In this case, both alleles are functional, but they ahve mutations that lead to difference in where they are expressed (or turned on). There are few examples of true co-cominant traits in reptiles, but classic examples include human blood type and roan coat color in horses and cattle.
MSN  jackson-yan@163.com

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MSN  jackson-yan@163.com

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謝謝   大大的解釋

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稍微貢獻一下好了
我翻譯好了 PO出來

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轉載蟒蛇基因
遺傳學
學習基本的遺傳學和育種者的reptilekeepers

由Vincent j的林奇

看來幾乎所有常見的爬行動物物種保存,繁殖hobbyistss這幾天至少有一個基因的顏色或圖案變形。對於某些物種,如球蟒,玉米蛇和豹壁虎,變種的數量是真正勢不可擋。這種普及增加了使用遺傳方面,它描述了如何變種被繼承和預測的結果對變形的十字架。不幸的是,變形爆炸還推出了混亂,有時甚至神秘的遺傳術語和數學到愛好。但爬行動物遺傳學突變的顏色和圖案沒有困難。一些生物學基礎使他們容易理解。

建立一個基礎
動物由億萬細胞組成。在每個細胞是一種特殊的個體稱為核心,它裡面的細胞的基因。這些基因的總和 - 以及它們之間的所有DNA - 被稱為基因組。除了精子和卵子,每個單元有兩個完整的動物的基因組複製。一個是繼承自母親,另一個來自父親。原則上每個複製的基因組的估計 60,000基因是完全相同的。但在現實中,一些小的差異之間。這些被稱為基因突變。



在生產過程中出現突變的生殖細胞。該基因組被複製並包裝成精子和卵子。這個過程幾乎是完美的,但錯誤發生。考慮複印件一張照片。試想影印複製,然後複製該副本。做這個時間足夠長,你會發現小瑕疵慢慢扭曲原始圖像。幸運的是,進化設計了一個錯誤檢查系統。就像一個好的校對,它比較基因組複製一個新的原始和糾正錯誤。然而,即使這個機制不健全。錯誤可能發生在近30億的地方,所以一些錯誤將漏網之魚。每一個新的精子和卵子含有少數的突變。

大多數突變發生在功能上不重要的基因組區域。他們不作任何貢獻,動物的健康和容貌。然而,基因突變破壞基因的正常功能。如果基因突變發生在重要的顏料生產,儲存或色素格局的形成,創建一個新的變形。

例如,結果從一個白化突變失活的基因稱為酪氨酸酶,這是至關重要的黑色色素的形成。但並非所有的突變是有害的。有些可以真正受益的有機體。考慮抗生素抗藥性的細菌。他們的抵抗莖形成了一種酶的突變,使抗生素分解。細菌的基因突變有一個強大的優勢時,接觸到抗生素。他們生存和繁殖 - 即使這是對我們人類不好的。

幸運的是,一個單一的基因突變很少導致嚴重錯誤的東西。記住,每個基因有兩個拷貝。如果一個副本去突變,備份補償和接管。這兩種形式的基因,一個正常的和一個突變,而這些其他形式被稱為等位基因。有些基因是顯性給別人,這意味著它們可以完全取消的影響,另一等位基因。

例如白化再次考慮。在這種情況下,有兩個等位基因。正常的等位基因是顯性突變的等位基因。這意味著既不是用兩個普通基因動物,也不是一個動物,一個正常和白化突變複製展品的特點。這兩種動物看起來完全正常。只有一兩個基因突變的動物將是一個患白化病。

假設一個基因只有兩個等位基因喜歡我們的白化。這對可以在四種可能的組合方式。讓我們把正常基因的白化基因“A”和突變的等位基因的“A”。等位基因可以合併為 AA級,AA級,AA和AA級。這些等位基因的組合被稱為基因型。aA和AA在本質上是一樣的,所以我們可以減少複雜性,有三種基因型:AA、Aa和aa。純合子個體具有相同的等位基因,如AA和AA級。混合等位基因雜合子動物,如Aa。

請記住,正常等位基因(A)是顯性突變等位基因(a)在我們的白化例子,所以這三個基因型能有一兩個亮相。這些外表被稱為表型。因為正常等位基因(A)可以完全取消突變等位基因(一),動物使用AA或AA看起來是一樣的。如果沒有一個有效的複製基因,動物在aa上會呈現白化。



橫斷(穿越)動物

能預測結果後,穿越兩個變種是有價值的工具。雖然這種權力是現代生物學的基礎,是不可能在19世紀後期。主要的突破是從細緻的工作奧地利修道士孟德爾和博物學家。命名為“遺傳學之父”。孟德爾豌豆栽培性狀與幾個變量,包括花色,種子顏色和形狀的種子。保持詳細記錄父母和子女的外觀來自超過 28,00十字架,他能作出概括的繼承和預測結果的十字架。

孟德爾;的工作幾乎被忽視了半世紀。直到1900年雷金納德 Punnet“重新發現”孟德爾的貢獻,把他們再拿出來使用。雖然 Punnet作出許多貢獻遺傳學領域,他是知道了發展 Punnet規矩,一個工具,用於預測後代的基因型和表型的基因型時,其父母是已知的。

利用白化動物的例子,讓我們穿過它與正常的動物。白化父母的基因型只能是AA級。假設正常的父母基因型為 AA。這意味著一個患白化病只能用精子或卵子的基因型A和動物的正常生殖細胞只能與 A基因型。如果您繁殖的動物,它們的後代繼承了A等位基因和A等位基因分別。攜帶 AA基因型,所有的雜合子後代為白化。

這個結果很容易預測,但結果變得更加複雜,當複雜因子動物,或“hets”,這些詞。這就是Punnet規矩變得非常方便。育種者可以用它確定的基因型和表型的後代,以及預測他們生產的概率。

我們的白化選育 hets例如產量三種可能的結果:aA,aa和AA。這個例子比較簡單,但跨越可以更加複雜。考慮製作一個設計變形,如白雪。這些動物被白化和anerythristic,字面意思是沒有 erythrin,紅色顏料。 “Anery”動物缺乏紅色,通常各種色調的黑色,白色和灰色。

最初的交叉生產正常進行的動物尋找一個等位基因為白化(a)和anery(R)的。換句話說,他們的基因型是AaRr,他們是雙重雜合子。

構建 Punnet廣場為雙過度緊張是類似於一個過度緊張(例如我們的白化病),除非我們現在有四個可能的基因型對精子和卵子:分析純,氬氣,氬氣和氬氣。而不是四個細胞和四種可能的結果對我們 Punnet規矩,我們有16個細胞,16種可能的結果。只有16個中其中一個白化基因。

事情變得複雜得多當三個基因參與。橫斷64個可能的基因型,只有一個展示你追求的特質。你可能得到的圖片。

更複雜的關卡

在我們的白化例子中,顯然等位基因顯性或隱性的,但情況並非總是如此。簡單的遺傳性狀(如白化和anerythristics)可以被解釋為顯性和隱性等位基因。複雜性狀無法解釋那麼容易。幾種複雜性狀出口,但只有少數是重要的爬行動物繁殖,如不完全顯性,共顯性,多基因遺傳性狀。

有時出現的雜合子(AA)的不同,都純合子(AA和AA)和存在於兩者之間的外觀兩種純合子。在這種情況下,既不等位基因能夠取消影響了其他的,所以其效果融為一體。這種類型的繼承被稱為不完全顯性。因為它發生突變改變這些基因的功能之一,但並沒有完全摧毀它。每個基因在hetrozygot將有助於東西的表型。

一個很好的例子已經表明不完全顯性性狀在玉米蛇。這些蛇有三個等位基因酪氨酸酶的基因:A和U 該基因負責製造的黑色素。AA個體都是正常的,aa是白化,uu是HYPO,這是一個非常極端的 - 近白化 - 形式hypomelanism。



在不完全顯性基因時出現白化(AA)的育成,是一個極端HYPO(UU)的。由於等位基因不能相互抵消,它們的後代有第三個表型,分裂的區別白化跟極端 hypo。這些“aU”的個人被稱為“ULTRA AMEL”或“ultramel”,並有更多的黑色素白化,但更比普通動物還多的黑色素。因此,等位基因A和U是不完全顯性到對方,但都是隱性的A

不同於不完全顯性性狀,性狀合作的優勢是特殊情況時表示,兩個等位基因都在同一時間,所以表型是一種混合物 - 不是交融 - 兩種純合子表型。在這種情況下,兩個等位基因的功能,但是他們有基因突變導致的差異在哪裡他們都表達了(或打開)。有幾個例子,真正的合作,cominant性狀的爬行動物,但典型的例子包括人類的血型和羅安毛色馬和牛。
↑↑↑↑↑↑↑↑↑↑↑↑↑↑↑↑↑↑↑↑↑↑↑↑↑↑↑↑↑↑↑↑↑
以上,抱歉,小弟英文不好,且有些專有名詞可能會翻錯
不過大致上就是A和a基因會配出(AA、Aa、aA-正常版)跟aa-白化版
裡面的U已經牽扯到色素的控制,小弟有看沒有懂~.~

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