Morphological features and inheritance of Foliaceous Stipules of primary leaves in cowpea (Vigna unguiculata)

BACKGROUND AND AIMS: The presence of connate foliaceous stipules of primary leaves and their inheritance in cowpea (Vigna unguiculata) genotype EC394736 is reported for the first time. METHODS: The development of foliaceous stipules (FS) and their persistence were examined throughout the growth and developmental stages of the plants of the genotype EC394736. The shape, size, colour, texture and other parameters were examined in the field during the period 15-50 d after sowing. The area of FS was measured using image analysis software. The inheritance of FS was studied by making a cross between the genotype EC394763 with rudimentary stipules (RS) and the genotype EC394736, which has connate foliaceous stipules of primary leaves. The presence or absence of FS in plants of the F1, F2 and F3 generations was recorded. KEY RESULTS: The stipules developed along with the primary leaves in the genotype EC394736. One stipule of each primary leaf fused with the adjacent stipule of the other primary leaf forming a foliaceous structure. These stipules persisted on the plants for >50 d, even after the primary leaves had withered off. The F1 plants showed an absence of FS indicating the rudimentary stipules to be dominant over foliaceous stipules. The F2 segregation into 15 (RS) : 1 (FS) indicated that duplicate recessive genes controlled the presence of the FS. This was confirmed from the segregation pattern in the F3 generation. CONCLUSIONS: The presence of FS is a unique feature in cowpea genotype EC394736 and duplicate recessive genes govern it. The FS can be used as a morphological marker for identification of cowpea varieties.     

The pvr1 locus in Capsicum encodes a translation initiation factor eIF4E that interacts with Tobacco etch virus VPg

Mutations in the eIF4E homolog encoded at the pvr1 locus in Capsicum result in broad-spectrum potyvirus resistance attributed to the pvr1 resistance allele, a gene widely deployed in agriculture for more than 50 years. We show that two other resistance genes, previously known to be eIF4E with narrower resistance spectra, pvr2(1) and pvr2(2), are alleles at the pvr1 locus. Based on these data and current nomenclature guidelines, we have re-designated these alleles, pvr1(1) and pvr1(2), respectively. Point mutations in pvr1, pvr1(1), and pvr1(2) grouped to similar regions of eIF4E and were predicted by protein homology models to cause conformational shifts in the encoded proteins. The avirulence determinant in this potyvirus system has previously been identified as VPg, therefore yeast two-hybrid and GST pull-down assays were carried out with proteins encoded by the pvr1 alleles and VPg from two different strains of Tobacco etch virus (TEV) that differentially infected Capsicum lines carrying these genes. While the protein encoded by the susceptible allele pvr1+ interacted strongly, proteins translated from all three resistance alleles (pvr1, pvr1(1), and pvr1(2)) failed to bind VPg from either strain of TEV. This failure to bind correlated with resistance or reduced susceptibility, suggesting that interruption of the interaction between VPg and this eIF4E paralog may be necessary, but is not sufficient for potyvirus resistance in vivo. Among the three resistance alleles, only the pvr1 gene product failed to bind m7-GTP cap-analog columns, suggesting that disrupted cap binding is not required for potyvirus resistance.     

Thrips tabaci and tomato spotted wilt virus: inheritance of vector competence

Populations of onion thrips, Thrips tabaci Lindeman (Thysanoptera: Thripidae), were shown to differ significantly in their ability to transmit an isolate of tomato spotted wilt virus (Tospovirus: Bunyaviridae) (TSWV) collected from potato [Solanum tuberosum L. (Solanaceae)]. To gain an understanding of the basis for this variation, we generated reciprocal crosses between an efficient and an inefficient transmitting population. The resulting F₁ progeny and progeny from the parental populations were tested for their ability to transmit TSWV. Our results indicate that the ability to transmit TSWV efficiently by T. tabaci is inherited as a recessive trait.     

Serine proteinase activation of latent human skin collagenase

Latent and active collagenase were demonstrated following direct extraction from normal skin homogenates with 0.1M calcium chloride at 60 degrees C. 83% of the collagenase activity was in latent form and could be maximally activated with trypsin. Partial activation of the latent enzyme could also be demonstrated by incubation of the skin extract without added trypsin. This endogenous activation was inhibited by the addition of soya bean trypsin inhibitor, trasylol, di-isopropylphosphofluoridate and phenylmethanesulphonylfluoride, none of which inhibited collagenase directly. This suggests that the skin extracts contain a collagenase activating enzyme with the inhibition profile of a serine proteinase. A chymotryptic proteinase with a similar inhibition profile was extracted from normal human skin and partially purified. This enzyme activated fibroblast procollagenase derived from tissue culture of normal skin. The procollagenase was also partially activated by plasmin and chymotrypsin. This is the first demonstration of a collagenase activating enzyme in human skin and raises the possibility that collagenase activation by this mechanism may be responsible for collagen degradation in some disease processes.     

cmv1 is a gate for Cucumber mosaic virus transport from bundle sheath cells to phloem in melon

Cucumber mosaic virus (CMV) has the broadest host range among plant viruses, causing enormous losses in agriculture. In melon, strains of subgroup II are unable to establish a systemic infection in the near‐isogenic line SC12‐1‐99, which carries the recessive resistance gene cmv1 from the accession PI 161375, cultivar ‘Songwhan Charmi’. Strains of subgroup I overcome cmv1 resistance in a manner dependent on the movement protein. We characterized the resistance conferred by cmv1 and established that CMV‐LS (subgroup II) can move from cell to cell up to the veins in the inoculated leaf, but cannot enter the phloem. Immunogold labelling at transmission electron microscopy level showed that CMV‐LS remains restricted to the bundle sheath (BS) cells in the resistant line, and does not invade vascular parenchyma or intermediary cells, whereas, in the susceptible line ‘Piel de Sapo’ (PS), the virus invades all vein cell types. These observations indicate that the resistant allele of cmv1 restricts systemic infection in a virus strain‐ and cell type‐specific manner by acting as an important gatekeeper for virus progression from BS cells to phloem cells. Graft inoculation experiments showed that CMV‐LS cannot move from the infected PS stock into the resistant cmv1 scion, thus suggesting an additional role for cmv1 related to CMV transport within or exit from the phloem. The characterization of this new form of recessive resistance, based on a restriction of virus systemic movement, opens up the possibility to design alternative approaches for breeding strategies in melon.     

Induced mutation to monocotyledony in periwinkle,Catharanthus roseus, and suppression of mutant phenotype by kinetin

A recessive EMS-induced mutation inherited in Mendelian fashion caused monocotyledonous embryo formation and seed germination on high salt medium inCatharanthus roseus. Availability during embryo development of exogenously supplied cytokinin kinetin suppressed the mutant phenotype. These observations suggest that, inC. roseus, (i) insufficiency in endogenous kinetin may lead to monocotyledonous embryo patterning and (ii) dicotyledonous embryo formation requires a critical amount of kinetin in certain cells of early embryos.     

Invited review: Bioinformatic methods to discover the likely causal variant of a new autosomal recessive genetic condition using genome-wide data

In animals, new autosomal recessive genetic diseases (ARGD) arise all the time due to the regular, random mutations that occur during meiosis. In order to reduce the effect of any damaging new variant, it is necessary to find its cause. To evaluate the best way of doing this, 34 papers which found the exact location of a new genetic disease in livestock were reviewed and found to require at least two stages. In the initial stage the commonly used χ² method, applied in a case-control association analysis with single nucleotide polymorphism (SNP)-chip data, was found to have limitations and was almost always used in conjunction with a second method to locate the target region on the genome containing the variant. The commonly used methods had their drawbacks; so a new method was devised based on long runs of homozygosity, a common feature of new ARGD. This ‘autozygosity by difference’ method was found to be as good as, or better than, all the reviewed methods tested based on its ability to unambiguously find the shortest known target region in an already analysed data set. Mean target region length was found to be 4.6 megabases in the published reports. Success did not depend on the size of commercial SNP-chip used, and studies with as few as three cases and four controls were large enough to find the target region. The final stage relied on either sequencing the candidate genes found in the target region or using whole genome sequencing (WGS) on a small number of cases. Sometimes this latter method was used in conjunction with WGS on a number of control animals or resources such as the 1000 bull genomes data. Calculations showed that, in cattle, less than 15 animals would be needed in order to locate the new variant when using WGS data. This could be any combination of cases plus parents or other unrelated animals in the breed. Using WGS data, it would be necessary to search the three billion bases of the cattle genome for base positions which were homozygous for the same allele in all cases and heterozygous for that allele in parents, or not containing that homozygote in unrelated controls. This site could be confirmed on other healthy animals using much cheaper methods, and then a genetic test could be devised for that variant in order to screen the whole population and to devise a breeding programme to eliminate the disorder from the population.     

PKHD1基因缺陷与常染色体隐性遗传性多囊肾病的研究进展

PKHD1是目前所知人类常染色体隐性遗传多囊肾病(autosomal recessive polycystic kidney disease,ARPKD)的惟一致病基因。ARPKD临床病变以双肾多发性进行性充液囊泡为主要特征。目前对PKHDl基因在ARPKD发病中的作用了解并不多。该文对ARPKD的发病机制和PKHD1基因功能最新研究进展进行综述。