Molecular genetic basis of Rhizobium–legume interactions

Genome ◽  
1989 ◽  
Vol 31 (1) ◽  
pp. 350-353 ◽  
Author(s):  
A. Kondorosi ◽  
E. Kondorosi ◽  
Z. Györgypal ◽  
Z. Banfalvi ◽  
J. Gyuris ◽  
...  

Recognition of the appropriate legume and nodule induction are controlled by common (nod) and host-specific nodulation (hsn) genes in Rhizobium. The nod and hsn genes are activated by the product of the regulatory nodD in conjunction with specific flavonoids excreted by the plant. Differences in the flavonoid specificity of the NodD proteins occur between different Rhizobium species, or between strains of a given species or even within one strain containing several copies of the nodD gene. Accordingly, the nodD gene controls the host-specific expression of nod and hsn genes. In addition, the nodulation genes are under not only positive but also negative regulation which is mediated by a nod-specific repressor protein. This dual control is required for optimal nodulation of the plant host. Further steps in nodule development are again controlled by the infecting Rhizobium. It was found that at least four different classes of Rhizobium fix genes are involved directly or indirectly in the expression of late nodulin genes, finally leading to the establishment of nitrogen-fixing symbiosis.Key words: Rhizobium meliloti, nodulation genes, plant signals, fix genes, alfalfa.

1998 ◽  
Vol 11 (5) ◽  
pp. 393-403 ◽  
Author(s):  
Pascal Gamas ◽  
Françoise de Billy ◽  
Georges Truchet

Two Medicago truncatula nodulin genes putatively encoding proteins structurally related to two classes of proteins commonly associated with plant defense reactions have been characterized. MtN1 is homologous to two small, cysteine-rich, pathogen-inducible proteins from pea (pI39 and pI230), whereas MtN13 is closely related to the PR10 family of pathogenesis-related proteins. We show that neither MtN1 nor MtN13 is induced in leaves in response to pathogenic bacteria, and that both are exclusively expressed during nodulation. In situ hybridization experiments as well as Northern (RNA) studies of interactions between M. truncatula and either wild-type Rhizobium meliloti or mutants deficient in infection establish that MtN1 is associated with the infection process, while MtN13 represents the first specific marker described for the nodule outer cortex. Possible roles for MtN1 and MtN13 are discussed. We also present the identification of another member of the PR10 family, designated as MtPR10-1, whose regulation is strikingly different from that observed for MtN13, being constitutively expressed in roots and pathogen-inducible in leaves.


1986 ◽  
Vol 160 (1) ◽  
pp. 69-75 ◽  
Author(s):  
Ilona DUSHA ◽  
Joachim SCHRODER ◽  
Peter PUTNOKY ◽  
Zsofia BANFALVI ◽  
Adam KONDOROSI

1992 ◽  
Vol 85 (2) ◽  
pp. 253-265 ◽  
Author(s):  
D. P. S. Verma ◽  
C.-A. Hu ◽  
M. Zhang

Genome ◽  
1989 ◽  
Vol 31 (1) ◽  
pp. 354-360 ◽  
Author(s):  
San Chiun Shen ◽  
Shui Ping Wang ◽  
Guan Qiao Yu ◽  
Jia Bi Zhu

Genes that specify nodulation (nod genes) are only active in the free-living rhizobia or in the nodule initiation state of rhizobia. As soon as the repression of nod genes occurs in the bacteroids of the nodule, nifA is induced, while ntrC is inactivated and thus the nifA-mediated nif/fix genes are turned on. Limitation of available oxygen brings about the induction of nifA, which reflects the actual status of nif/fix gene activities in symbiotic state of rhizobia. Oxygen thus appears to be a major symbiotic signal to the expression of bacteroid nif/fix genes. Mutation of nifA or shortage of nifA product in wild-type rhizobia caused by the inhibition of multicopy nifH/fixA promoters leads to an abnormal development of nodules and premature degradation of bacteroids in nodules.Key words: nitrogen fixation, nodulation, nif/fix regulation, nifA mutant.


2005 ◽  
Vol 26 (2) ◽  
pp. 251-282 ◽  
Author(s):  
Héctor F. Escobar-Morreale ◽  
Manuel Luque-Ramírez ◽  
José L. San Millán

The genetic mechanisms underlying functional hyperandrogenism and the polycystic ovary syndrome (PCOS) remain largely unknown. Given the large number of genetic variants found in association with these disorders, the emerging picture is that of a complex multigenic trait in which environmental influences play an important role in the expression of the hyperandrogenic phenotype. Among others, genomic variants in genes related to the regulation of androgen biosynthesis and function, insulin resistance, and the metabolic syndrome, and proinflammatory genotypes may be involved in the genetic predisposition to functional hyperandrogenism and PCOS. The elucidation of the molecular genetic basis of these disorders has been burdened by the heterogeneity in the diagnostic criteria used to define PCOS, the limited sample size of the studies conducted to date, and the lack of precision in the identification of ethnic and environmental factors that trigger the development of hyperandrogenic disorders. Progress in this area requires adequately sized multicenter collaborative studies after standardization of the diagnostic criteria used to classify hyperandrogenic patients, in whom modifying environmental factors such as ethnicity, diet, and lifestyle are identified with precision. In addition to classic molecular genetic techniques such as linkage analysis in the form of a whole-genome scan and large case-control studies, promising genomic and proteomic approaches will be paramount to our understanding of the pathogenesis of functional hyperandrogenism and PCOS, allowing a more precise prevention, diagnosis, and treatment of these prevalent disorders.


PLoS ONE ◽  
2016 ◽  
Vol 11 (11) ◽  
pp. e0164359 ◽  
Author(s):  
Luis Zea ◽  
Nripesh Prasad ◽  
Shawn E. Levy ◽  
Louis Stodieck ◽  
Angela Jones ◽  
...  

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