Recessivity, resistance genes

Resistance genes can be dominant, recessive, incompletely dominant, or incompletely recessive. Resistance to carbamates and organophosphates is usually dominant or incompletely dominant. Resistance to DDT, Bt, and spinosyns is usually recessive. Resistance to dieldrin is usually incompletely dominant. Resistance to pyrethroids is usually incompletely recessive. As shown in Figure 10.1 and 10.2, diamondback moth resistance to per-methrin was inherited as an incompletely recessive, autosomal factor, whereas resistance to methomyl was inherited as an incompletely dominant, autosomal factor. In cases of monofactorial inheritance of resistance to insecticides, the degree of dominance (D) in the progeny can be calculated, as described by Stone (1968), as follows ... 

To estimate the relative fitness of the genotypes, dicofol resistance was modelled as a monogenic, recessive trait (22) and it was assumed that any fitness cost associated with the resistance gene would also be recessive. Allelic frequencies for the resistance alleles, R and S, are denoted by q and p, respectively. 

Nephrogenic diabetes insipidus (NDI) is characterized by renal tubular resistance to the antidiuretic effect of arginine vasopressin (AVP). NDI may be inherited as an autosomal dominant or X-linked recessive disorder. The autosomal dominant form of NDI results from mutations of the aquaporin 2 gene (AQP2). AQP2 encodes a water channel of the renal collecting duct. Its disruption causes autosomal dominant NDI (113,114) and occasionally recessive forms of the disease. 

The antibiotic fusidic acid inhibits protein synthesis by preventing EF-G from cycling off of the ribosome. Fusidic-acid-resistant mutants of EF-G have been isolated. Fusidic acid resistance is recessive to sensitivity. In other words, an E. coli cell containing two EF-G genes, one resistant and one sensitive, is still sensitive to the antibiotic. Why Hint Look at fig. 29.2.)... 

Cioli, D., Pica-Mattoccia, L. and Moroni, R. (1992) Schistosoma mansoni hycanthone/oxamniquine resistance is controlled by a single autosomal recessive gene. Experimental Parasitology 75, 425 432. 

By this approach, positive clones are expected to arise from overexpression of wild-type genes conferring resistance or from frans-dominant mutations giving a mutant (resistant) phenotype (14). To identify loss-of-function recessive mutations the method should be reversed P-RES resistant clones should be transformed with a genomic library constructed with the DNA of the wild-type HB101, and clones with restored peptide susceptibility analyzed. 

Several disorders of tubular phosphate handhng have been described. The best known of these is X-linked dominant hypophosphatemic rickets (previously known as vitamin D-resistant rickets). This disorder arises because of a defect in the PHEX gene. A defect of the sodium-dependent/ phosphate co-transporter has also been described, giving rise to autosomal recessive hereditary hypophosphatemic rickets with hypercalciuria. The molecular biology of tliese and other renal phosphate transport disorders has been reviewed. ... 

An autosomal recessive disease known as hereditary vitamin D-resistant riekets, type II is caused by defects in the gene for the vitamin D receptor which renders it nonfunctional. Thus, this knockout of VDR function illustrates its importance. Patients with this disease have high circulating levels of 1,25-(OH)2D (unlike type 1 disease which is due to la-hydroxylase deficiency, discussed earlier), severe rickets, and alopecia. The alopecia may... 

The AXRl pathway. Genetic studies indicate that four of the Arabidopsis auxin-response genes (AXRl, TIRl, AXR4, and SARI) function in the same or overlapping pathways. The recessive axrl mutations confer auxin resistance as well as diverse morphological defects... 

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