The rlt11 and raec1 mutants of Arabidopsis thaliana lack the activity of a basic-amino-acid transporter

The concentration dependence of the influx of L-lysine in excised roots of Arabidopsis thaliana seedlings was analyzed for the wild-type (WT) and two mutants, rlt11 and raec1, which had been selected as resistant to lysine plus threonine, and to S-2-aminoethyl-L-cysteine, respectively. In the WT three components were resolved: (i) a high-affinity, low-capacity component [K-m=2.2 mu M; V-max=23 nmol .(g FW)(-1). h(-1)]; (ii) a low-affinity, high-capacity component [K-m=159 mu M; V-max=742 nmol .(g FW)(-1). h(-1)]; (iii) a component which is proportional to the external concentration, with a constant of proportionality k=104 nmol .(g FW)(-1). h(-1). mM(-1). The influx of L-lysine in the mutants was lower than in the WT, notably in the concentration range 0.1-0.4 mM, where it was only 7% of that in the WT. In both mutants the reduced influx could be fully attributed to the absence of the low-affinity (high-K-m) component. This component most likely represents the activity of a specific basic-amino-acid transporter, since it was inhibited by several other basic amino acids (arginine, ornithine, hydroxylysine, aminoethylcysteine) but not by L-valine. The high-affinity uptake of L-lysine may be due to the activity of at least two general amino acid transporters, as it was inhibitable by L-valine, and could be further dissected into two components with a high affinity (K-i=1-5 mu M) and a low affinity (K-i=0.5-1 mM) for L-valine, respectively. The rlt11 and raec1 mutant have the same phenotype and the corresponding loci were mapped on chromosome 1, but it is not yet clear whether they are allelic

The raz1 mutant of Arabidopsis thaliana lacks the activity of a high-affinity amino acid transporter

The raz1 mutant of Arabidopsis thaliana (L.) Heynh. has been selected as resistant to the toxic proline analogue, azetidine-2-carboxylic acid (2AZ). Seedlings of the mutant tolerated fivefold higher concentrations of 2AZ (ED(50) = 0.25 mM) than the wild-type seedlings (ED(50) = 0.05 mM). The mutant gene was found to be semi-dominant and the corresponding RAZ1 locus was mapped on chromosome 5 at 69.6 +/- 1.8 cM. The resistance to 2AZ could be fully and exclusively accounted for by the lower uptake rate of the proline analogue in the mutant. The influx of L-proline in roots of wild-type seedlings could be dissected into two components: (i) a component with a high affinity and a low capacity for L-proline (K-m approximate to 20 mu M, V-max approximate to 60 nmol .(g FW)(-1). h(-1)) and also a high affinity for r-2AZ (K-i approximate to 40 mu M) and (ii) a low-affinity, high-capacity component (K-m approximate to 5 mM: V-max = 1300 nmol .(g FW)(-1). h(-1)). Clearly, the raz1 mutation affects the activity of a high-affinity transporter, because the high-affinity uptake of proline in the mutant was at least fivefold lower than in the wild-type, whereas the low-affinity uptake was unchanged

Does abdominal obesity cause increase in the amount of epidural fat?

It is known that epidural fat does not alter in obese people. This study aims to find out a possible relationship with epidural fat and abdominal obesity. In this cross-sectional study, 63 patients who were referred to our clinic for lumbar magnetic resonance imaging (MRI) examination were evaluated. Patients with the history of steroid treatment, thyroid disease or Cushing disease were excluded. Waist circumferences (WC), body weight and height were measured and subsequently body-mass index (BMI) was calculated (kg/m²). On midsagittal T1-weighted images, anterior epidural fat (AEF), posterior epidural fat (PEF) and posterior subcutaneous fat (SCF) thicknesses were measured at the S1 level. The results were compared with age, gender, body weight, height, WC and BMI. There were 31 men and 32 women, age ranged 19–77 years (mean 49). The mean BMI was 29.25 kg/m² (20.7–52.7); the mean WC was 97.4 ± 13.2 cm (72–122) in women and 97.6 ± 9.8 cm (72–118) in men. Cutoff value of WC was considered as 88 cm for women and 95 cm for men. BMI > 27.5 was considered to be obese. No statistical difference with respect to epidural fat thickness between genders was determined in AEF and PEF (P = 0.237, P = 0.616). SCF was significantly thicker in women (P = 0.021). A very poor and negative correlation was found between age and PEF (r = 0.373, P = 0.003), and a very poor and positive correlation between weight and PEF was found (r = 396, P = 0.001). The thickness of the epidural fat was not differ between obese and nonobese people (p = 0.571 for AEF and p = 0.307 for PEF). The thickness of the epidural fat was not different in people whose WC was greater than normal values in both gender (p > 0.05). Epidural fat is not affected by age, gender, BMI and WC which means that epidural fatty layer. A clear correlation has not been found between epidural fat amount and obesity or abnormal fat distribution yet