Analysis of the chicken genome : mapping of monogenic traits

The development of genetic linkage maps in farm animals is progressing rapidly. Linkage maps can be used to identify genetic loci responsible for genetic variation in traits of economic importance. The ultimate goal is to find the underlying genes involved in these traits. To achieve this, the so called positional candidate gene approach is gaining in importance. This approach is based on the genetic localization of a trait using genetic linkage analysis in livestock species. Subsequent comparative mapping of the trait locus with the gene-rich maps of the human and the mouse may reveal candidate genes for the trait in question.For the construction of comparative maps the genetic localization of many genes needs to be determined. In this thesis, the development of highly informative microsatellite markers from expressed sequences, derived from a brain and embryonic cDNA library of the chicken, is described. In addition to this, a preliminary comparative map of the chicken is presented.The second objective of this thesis was to develop a quick and reliable method in order to localize monogenic traits. To achieve this, an already existing technique, called bulked segregant analysis, which has originally been used for the localization of monogenic traits in plants using random amplified polymorphic DNA markers (RAPDs), and restriction fragment length polymorhisms (RFLPs), was combined with the use of fluorescently labelled microsatellite markers. This method prooved to be very sensitive in detecting linked markers at greater genetic distances and the genetic map locations of the monogenic traits Dominant White ( I ) and Autosomal dwarfism ( adw ) were succesfully determined.Comparative mapping revealed that adw is located in a chromosomal region that is conserved between chicken, human and mouse. Interestingly, in the mouse the phenotype "Pygmy" , which shows a striking similarity to the Autosomal Dwarf phenotype in chickens, is also located in this region. The Pygmy phenotype arises from the inactivation of the High Mobility Group I-C ( HMGI-C ) gene. In the human, the HMGI-C gene is also located in the same conserved chromosomal segment. Fluorescent in situ hybridization of chicken metaphase chromosomes using the chicken HMGI-C gene as a probe, showed that the chicken HMGI-C gene is indeed located in the region of the adw locus. However, northern blot analysis showed no difference in the expression of the HMGI-C gene between adw and wild type chicken embryos. Also no mutations in the HMGI-C mRNA were detected. Finally, other candidate genes for both adw and I are proposed.</p

The interaction between strigolactones and other plant hormones in the regulation of plant development : Review

Plant hormones are small molecules derived from various metabolic pathways and are important regulators of plant development. The most recently discovered phytohormone class comprises the carotenoid-derived strigolactones (SLs). For a long time these compounds were only known to be secreted into the rhizosphere where they act as signaling compounds, but now we know they are also active as endogenous plant hormones and they have been in the spotlight ever since. The initial discovery that SLs are involved in the inhibition of axillary bud outgrowth, initiated a multitude of other studies showing that SLs also play a role in defining root architecture, secondary growth, hypocotyl elongation, and seed germination, mostly in interaction with other hormones. Their coordinated action enables the plant to respond in an appropriate manner to environmental factors such as temperature, shading, day length, and nutrient availability. Here, we will review the current knowledge on the crosstalk between SLs and other plant hormones—such as auxin, cytokinin, abscisic acid (ABA), ethylene (ET), and gibberellins (GA)—during different physiological processes. We will furthermore take a bird's eye view of how this hormonal crosstalk enables plants to respond to their ever changing environments

Distinct roles for strigolactones in cyst nematode parasitism of Arabidopsis roots

Phytohormones play an essential role in different stages of plant-nematode interactions. Strigolactones (SLs) are a novel class of plant hormones which play an important role in plant development. Furthermore, certain soil-inhabiting organisms exploit this plant molecule as allelochemical. However, whether SLs play a role in plant parasitism by nematodes is as yet unknown. This prompted us to investigate the potential role of SLs in different stages of the nematode life cycle using the beet cyst nematode Heterodera schachtii and Arabidopsis as a model system. We analyzed the effect of SLs on cyst nematode hatching, host attraction and invasion, and the establishment of a feeding relation upon infection of the SL deficient mutant max4-1 and the SL signaling mutant max2-1. In addition, infection assays were performed under phosphate shortage to enhance SL production and in the presence of the synthetic SL analog GR24. From this study, we can conclude that SLs do not contribute to cyst nematode hatching at the levels tested but that they do play a role in host attraction and subsequent invasion in a MAX2 dependent manner. Furthermore, we observed that increased levels of exogenous and endogenous SLs change the root invasion zone. Upon root infection, cyst nematode development was enhanced in both the max2-1 and max4-1 mutants due to the formation of enlarged feeding cells. These data provide evidence for distinct roles of SLs during cyst nematode parasitism of plant roots

The role of strigolactones in P deficiency induced transcriptional changes in tomato roots

BACKGROUND: Phosphorus (P) is an essential macronutrient for plant growth and development. Upon P shortage, plant responds with massive reprogramming of transcription, the Phosphate Starvation Response (PSR). In parallel, the production of strigolactones (SLs)—a class of plant hormones that regulates plant development and rhizosphere signaling molecules—increases. It is unclear, however, what the functional link is between these two processes. In this study, using tomato as a model, RNAseq was used to evaluate the time-resolved changes in gene expression in the roots upon P starvation and, using a tomato CAROTENOID CLEAVAGE DIOXYGENASES 8 (CCD8) RNAi line, what the role of SLs is in this. RESULTS: Gene ontology (GO)-term enrichment and KEGG analysis of the genes regulated by P starvation and P replenishment revealed that metabolism is an important component of the P starvation response that is aimed at P homeostasis, with large changes occurring in glyco-and galactolipid and carbohydrate metabolism, biosynthesis of secondary metabolites, including terpenoids and polyketides, glycan biosynthesis and metabolism, and amino acid metabolism. In the CCD8 RNAi line about 96% of the PSR genes was less affected than in wild-type (WT) tomato. For example, phospholipid biosynthesis was suppressed by P starvation, while the degradation of phospholipids and biosynthesis of substitute lipids such as sulfolipids and galactolipids were induced by P starvation. Around two thirds of the corresponding transcriptional changes depend on the presence of SLs. Other biosynthesis pathways are also reprogrammed under P starvation, such as phenylpropanoid and carotenoid biosynthesis, pantothenate and CoA, lysine and alkaloids, and this also partially depends on SLs. Additionally, some plant hormone biosynthetic pathways were affected by P starvation and also here, SLs are required for many of the changes (more than two thirds for Gibberellins and around one third for Abscisic acid) in the gene expression. CONCLUSIONS: Our analysis shows that SLs are not just the end product of the PSR in plants (the signals secreted by plants into the rhizosphere), but also play a major role in the regulation of the PSR (as plant hormone). SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12870-021-03124-0

A Novel Loss-of-Function Variant in Transmembrane Protein 263 (TMEM263) of Autosomal Dwarfism in Chicken

Autosomal dwarfism (adw) in chickens is a growth deficiency caused by a recessive mutation. Characteristic for adw is an approximately 30% growth reduction with short shank. The adw variant was first recognized in the Cornell K-strain of White Leghorns, but the genetic causal variant remained unknown. To identify the causal variant underlying the adw phenotype, fine mapping was conducted on chromosome 1, within 52–56 Mb. This region was known to harbor the causal variant from previous linkage studies. We compared whole-genome sequence data of this region from normal-sized and adw chickens in order to find the unique causal variant. We identified a novel nonsense mutation NP_001006244.1:p.(Trp59∗), in the transmembrane protein 263 gene (TMEM263), completely associated with adw. The nonsense mutation truncates the transmembrane protein within the membrane-spanning domain, expected to cause a dysfunctional protein. TMEM263 is reported to be associated with bone mineral deposition in humans, and the protein shows interaction with growth hormone 1 (GH1). Our study presents molecular genetic evidence for a novel loss-of-function variant, which likely alters body growth and development in autosomal dwarf chicken