该生物由一个DNA分子组成能做基因工程的载体么

当然可以
多细胞生物也是同样如此。你身体里面的每一个细胞都包含整套的基因组。（少数奇葩如红细胞或者生殖细胞另讲）

顶顶

单细胞生物是无性生殖，一般为溢裂。DNA都是一分为二的。所以单细胞生物能包含该生物全部基因
　　　　　　　　 --人活着本来就没什么意义，但只有活下去，才能找到有趣的事物…就像你找到了这朵花，就像我找到了你。

@wanyifei0123 效应B细胞里有控制合成相应抗体的基因，人体内的消灭所有病毒基因是都有了。 （还没出现的新病毒 的相应抗体 的基因也存在）
B细胞变成效应B细胞时 没有发生基因突变。
因为人体的基因是真核基因，含有内含子结构，而外显子的不同组合就能表达出不同的蛋白质，即一因多效，所以真正的情况是合成抗体的一个基因，通过外显子的不同组合方式就能合成多种不同的抗体。所以说基因原来就存在的。
　　　　　　　　 --人活着本来就没什么意义，但只有活下去，才能找到有趣的事物…就像你找到了这朵花，就像我找到了你。

@萌皇妖孽
。。。。。我也不查文献了。。也直接上百科吧
Somatic hypermutation
Somatic hypermutation (or SHM) is a cellular mechanism by which the immune system adapts to the new foreign elements that confront it (eg. microbes), as seen during class switching. A major component of the process of affinity maturation, SHM diversifies B cell receptors used to recognize foreign elements (antigens) and allows the immune system to adapt its response to new threats during the lifetime of an organism.[1] Somatic hypermutation involves a programmed process of mutation affecting the variable regions of immunoglobulin genes. Unlike germline mutation, SHM affects only individual immune cells, and the mutations are not transmitted to offspring.[2]
Mistargeted somatic hypermutation is a likely mechanism in the development of B-cell lymphomas.
When a B cell recognizes an antigen, it is stimulated to divide (or proliferate). During proliferation, the B cell receptor locus undergoes an extremely high rate of somatic mutation that is at least 105-106 fold greater than the normal rate of mutation across the genome. Variation is mainly in the form of single base substitutions, with insertions and deletions being less common. These mutations occur mostly at “hotspots” in the DNA, known as hypervariable regions. These regions correspond to the complementarity determining regions; the sites involved in antigen recognition on the immunoglobulin.The exact nature of this targeting is poorly understood, although is thought to be controlled by a balance of error-prone and high fidelity repair. This directed hypermutation allows for the selection of B cells that express immunoglobulin receptors possessing an enhanced ability to recognize and bind a specific foreign antigen.
Experimental evidence supports the view that the mechanism of SHM involves deamination of cytosine to uracil in DNA by an enzyme called Activation-Induced (Cytidine) Deaminase, or AID.[6][7] A cytosine:guanine pair is thus directly mutated to a uracil:guanine mismatch. Uracil residues are not normally found in DNA, therefore, to maintain the integrity of the genome most of these mutations must be repaired by high-fidelity DNA mismatch repair enzymes. The uracil bases are removed by the repair enzyme, uracil-DNA glycosylase.[7] Error-prone DNA polymerases are then recruited to fill in the gap and create mutations.[6][8]
The synthesis of this new DNA involves error-prone DNA polymerases, which often introduce mutations either at the position of the deaminated cytosine itself or neighboring base pairs. During B cell division the immunoglobulin variable region DNA is transcribed and translated. The introduction of mutations in the rapidly proliferating population of B cells ultimately culminates in the production of thousands of B cells, possessing slightly different receptors and varying specificity for the antigen, from which the B cell with highest affinities for the antigen can be selected. The B cells with the greatest affinity will then be selected to differentiate into plasma cells producing antibody and long-lived memory B cells contributing to enhanced immune responses upon reinfection.[2]
The hypermutation process also utilizes cells that auto-select against the 'signature' of an organism's own cells. It is hypothesized that failures of this auto-selection process may also lead to the development of an auto-immune response.

可以，自己都说单细胞了，那它要不包括…那不死了