Heredity
The word Hérédité is a loan (towards 1050) with the Latin hereditas (“that which one inherits”, with the concrete and abstract direction).
The Hérédité is the transmission of characteristics of the ancestors to their descendants, whatever the mode of this transmission. Generally, one indicates by heredity the transmission of biological characters.
Well before being included within a biological framework, the hereditary transmission described a legal fact: a Stronghold, a title, an office could be hereditary, i.e. transmitted by heritage. It is thus necessary to be very careful in the use of this term. It is right to say that the trade is hereditary in a company where one is blacksmith of wire father. That does not mean of course that the descendants are genetically blacksmiths.
One can make the distinction between social Heredity (or acquired) and genetic Heredity (or innate).
In acquired Heredity, one will find all the characters except genetics which come from the imitation or the opposition to the parents and attended social environment: the native tongue, culture, values, the trade, fortune, political ideas….
Innate Heredity relates to only the genetic characters transmitted by the parents.
Mendel and genetics
The discipline which studies biological heredity is the Génétique. It is a recent discipline, which was constituted during XIXe and XXe centuries, progressively of the conceptual and experimental discoveries.
At the 19th century, Mendel formula and shows rules of transmission of the characters, the Lois of Mendel, which are at the base of the formal Génétique. In parallel, the first experiments of cellular Biologie show the importance of the Chromosome S in this transmission of the characters.
It was necessary to await in 1943 the demonstration by Oswald Avery that DNA was well the genetic data carrier, and the discovery of its structure in double helix by Watson and Crick in 1953, to start to include/understand the molecular bases Lois of Mendel.
Various modes of transmission biological of the characters
The Hérédité mendélienne governs the majority of the characters.At the organizations diploïdes like the human S, each individual has two copies of each Gène, a copy coming from the mother and the other of the father (exception: genes of the sexual chromosomes). If these two versions are identical, the individual is known as Homozygote for gene considered. In the contrary case, it has two different versions (two different alleles), and it is known as Hétérozygote for this gene.
For example, a child having twice the Allèle “has” for gene of the Blood group will be of group has, whereas a child hétérozygote with an allele “has” and an allele “B” is of group AB. These two alleles are also expressed: one speaks about codominance. But all the alleles are not codominants: the allele O (zero, i.e. not of marker) is not it. A homozygote “O/O” is of group O, but a hétérozygote “A/O” is of group has, “B/O” of group B. One says that the allele O is recessive, and the alleles has and B dominating S compared to O.
There exist characters which do not follow the laws of the genetics mendélienne, one speaks then about Hérédité non-mendélienne.
It can be a question of a form of heredity extranucléaire, which corresponds to the transmission of the characters related to the DNA present not in the core but in Organite S at double membranes like the Mitochondrie S (organoids of the cellular Respiration) and the Chloroplaste S (organoids of the chlorophyllian Photosynthèse ). In general these organoids are brought by the Ovule. For example, the human Spermatozoïde leaves its mitochondries out of the ovule at the time of the Fécondation. The characters result thus from the maternal mitochondries: one speaks about transmission mitochondriale matrilinéaire. One finds this hereditary mode of transmission in the Maladies mitochondriales.
There exists also another way of qualified heredity of cytoplasmic heredity where they are components as the Protéine S which are transmitted. It is the case for the transmission of ESB and other diseases with prion S.
Internal bonds
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