Inheritance pattern and selection criteria for resistance to soybean cyst nematode races 3 and 9

The objective of this work was to determine soybean resistance inheritance to Heterodera glycines Ichinohe (soybean cyst nematode - SCN) races 3 and 9, as well as to evaluate the efficiency of direct and indirect selection in a soybean population of 112 recombinant inbred lines (RIL) derived from the resistant cultivar Hartwig. The experiment was conducted in a completely randomized design, in Londrina, PR, Brazil. The estimated narrow-sense heritabilities for resistance to races 3 and 9 were 80.67 and 77.97%. The genetic correlation coefficient (r g = 0.17; p<0.01) shows that some genetic components of resistance to these two races are inherited together. The greatest genetic gain by indirect selection was obtained to race 9, selecting to race 3 due to simpler inheritance of resistance to race 9 and not because these two races share common resistance genes. The resistance of cultivar Hartwig to races 3 and 9 is determined by 4 and 2 genes, respectively. One of these genes confers resistance to both races, explaining a fraction of the significant genetic correlation found between resistance to these SCN races. The inheritance pattern described indicates that selection for resistance to SCN must be performed for each race individually.

Report on a review of selected general and application controls over the State University of Iowa MAUI Student Financial Aid system for the period May 19, 2014 through July 31, 2014

Report on a review of selected general and application controls over the State University of Iowa MAUI Student Financial Aid system for the period May 19, 2014 through July 31, 2014

Report on a review of selected general and application controls over the Iowa State University of Science and Technology Kuali Financial System for the period April 30, 2014 through May 28, 2014

Report on a review of selected general and application controls over the Iowa State University of Science and Technology Kuali Financial System for the period April 30, 2014 through May 28, 2014

Report on a review of selected general and application controls over the University of Northern Iowa Facility Administration and Maintenance Information System for the period April 29, 2014 through June 5, 2014

Report on a review of selected general and application controls over the University of Northern Iowa Facility Administration and Maintenance Information System for the period April 29, 2014 through June 5, 2014

Inheritance of resistance to soybean cyst nematode races 3 and 14 in soybean RIL and F2 populations

The objective of this work was to evaluate the soybean inheritance of resistance to cyst nematode races 3 and 14. The following populations where evaluated: one population of recombinant inbred lines (RILs) [Hartwig (resistant) x Y23 (susceptible line)] for races 3, 14 and 9; one population of families F2:3 [M-SOY 8001 (resistant) x MB/BR 46 - Conquista (susceptible)] for race 3; and one population of families F2:3 [(S5995 (resistant) x BRSMG Renascença (susceptible)] for race 14. In RIL populations, four epistatic genes were identified which conditioned resistance to race 14, and three epistatic ones for resistance to races 3 and 9. The lack of one gene provided moderate resistance under all situations. The highest number of genes for resistance to race 14 points out that genes responsible for lower effects might be involved. In population F2:3 from M-SOY 8001 x MB/BR 46 - Conquista, one recessive gene for moderate resistance and two recessive genes complete resistance to race 3 were identified. Two recessive genes conditioning moderate resistance to race 14 were identified in population F2:3 from the crossing S5995 x BRSMG Renascença. These results will be useful in designing crossings, involving these parentals, with higher possibility to accumulating genes that provide resistance to several SCN races.

Type I IFN controls chikungunya virus via its action on nonhematopoietic cells.

Chikungunya virus (CHIKV) is the causative agent of an outbreak that began in La Réunion in 2005 and remains a major public health concern in India, Southeast Asia, and southern Europe. CHIKV is transmitted to humans by mosquitoes and the associated disease is characterized by fever, myalgia, arthralgia, and rash. As viral load in infected patients declines before the appearance of neutralizing antibodies, we studied the role of type I interferon (IFN) in CHIKV pathogenesis. Based on human studies and mouse experimentation, we show that CHIKV does not directly stimulate type I IFN production in immune cells. Instead, infected nonhematopoietic cells sense viral RNA in a Cardif-dependent manner and participate in the control of infection through their production of type I IFNs. Although the Cardif signaling pathway contributes to the immune response, we also find evidence for a MyD88-dependent sensor that is critical for preventing viral dissemination. Moreover, we demonstrate that IFN-alpha/beta receptor (IFNAR) expression is required in the periphery but not on immune cells, as IFNAR(-/-)-->WT bone marrow chimeras are capable of clearing the infection, whereas WT-->IFNAR(-/-) chimeras succumb. This study defines an essential role for type I IFN, produced via cooperation between multiple host sensors and acting directly on nonhematopoietic cells, in the control of CHIKV.

Report on a review of selected general and application controls over the Iowa Department of Human Services’ Iowa Collection and Reporting System (ICAR) for the period April 1, 2013 through April 24, 2013 and April 1, 2014 through April 29, 2014

Report on a review of selected general and application controls over the Iowa Department of Human Services’ Iowa Collection and Reporting System (ICAR) for the period April 1, 2013 through April 24, 2013 and April 1, 2014 through April 29, 2014

Report on a review of selected general and application controls over the Iowa Department of Human Services’ Targeted Case Management System (TCM) for the period March 31, 2014 through April 18, 2014

Report on a review of selected general and application controls over the Iowa Department of Human Services’ Targeted Case Management System (TCM) for the period March 31, 2014 through April 18, 2014

Report on a review of selected general and application controls over the Iowa Department of Human Services’ Kindertrack System for the period March 30, 2015 through April 17, 2015

Report on a review of selected general and application controls over the Iowa Department of Human Services’ Kindertrack System for the period March 30, 2015 through April 17, 2015

Report on a review of selected general and application controls over the State University of Iowa PeopleSoft Human Resources Information System (HRIS) for the period May 11, 2015 through July 31, 2015

Report on a review of selected general and application controls over the State University of Iowa PeopleSoft Human Resources Information System (HRIS) for the period May 11, 2015 through July 31, 2015

ERK1/2 controls Na,K-ATPase activity and transepithelial sodium transport in the principal cell of the cortical collecting duct of the mouse kidney.

The collecting duct of normal kidney exhibits significant activity of the MEK1/2-ERK1/2 pathway as shown in vivo by immunostaining of phosphorylated active ERK1/2 (pERK1/2). The MEK1/2-ERK1/2 pathway controls many different ion transports both in proximal and distal nephron, raising the question of whether this pathway is involved in the basal and/or hormone-dependent transepithelial sodium reabsorption in the principal cell of the cortical collecting duct (CCD), a process mediated by the apical epithelial sodium channel and the basolateral sodium pump (Na,K-ATPase). To answer this question we used ex vivo microdissected CCDs from normal mouse kidney or in vitro cultured mpkCCDcl4 principal cells. Significant basal levels of pERK1/2 were observed ex vivo and in vitro. Aldosterone and vasopressin, known to up-regulate sodium reabsorption in CCDs, did not change ERK1/2 activity either ex vivo or in vitro. Basal and aldosterone- or vasopressin-stimulated sodium transport was down-regulated by the MEK1/2 inhibitor PD98059, in parallel with a decrease in pERK1/2 in vitro. The activity of Na,K-ATPase but not that of epithelial sodium channel was inhibited by MEK1/2 inhibitors in both unstimulated and aldosterone- or vasopressin-stimulated CCDs in vitro. Cell surface biotinylation showed that intrinsic activity rather than cell surface expression of Na,K-ATPase was controlled by pERK1/2. PD98059 also significantly inhibited the activity of Na,K-ATPase ex vivo. Our data demonstrate that the ERK1/2 pathway controls Na,K-ATPase activity and transepithelial sodium transport in the principal cell and indicate that basal constitutive activity of the ERK1/2 pathway is a critical component of this control.

Report on a review of selected general and application controls over the Iowa Public Employees’ Retirement System (IPERS) I-QUE Pension Administration System for the period April 9, 2015 through May 7, 2015

Report on a review of selected general and application controls over the Iowa Public Employees’ Retirement System (IPERS) I-QUE Pension Administration System for the period April 9, 2015 through May 7, 2015

N-myc controls proliferation, morphogenesis, and patterning of the inner ear

Myc family members play crucial roles in regulating cell proliferation, size, and differentiation during organogenesis. Both N-myc and c-myc are expressed throughout inner ear development. To address their function in the mouse inner ear, we generated mice with conditional deletions in either N-myc or c-myc. Loss of c-myc in the inner ear causes no apparent defects, whereas inactivation of N-myc results in reduced growth caused by a lack of proliferation. Reciprocally, the misexpression of N-myc in the inner ear increases proliferation. Morphogenesis of the inner ear in N-myc mouse mutants is severely disturbed, including loss of the lateral canal, fusion of the cochlea with the sacculus and utriculus, and stunted outgrowth of the cochlea. Mutant cochleas are characterized by an increased number of cells exiting the cell cycle that express the cyclin-dependent kinase inhibitor p27Kip1 and lack cyclin D1, both of which control the postmitotic state of hair cells. Analysis of different molecular markers in N-myc mutant ears reveals the development of a rudimentary organ of Corti containing hair cells and the underlying supporting cells. Differentiated cells, however, fail to form the highly ordered structure characteristic for the organ of Corti but appear as rows or clusters with an excess number of hair cells. The Kölliker's organ, a transient structure neighboring the organ of Corti and a potential source of ectopic hair cells, is absent in the mutant ears. Collectively, our data suggest that N-myc regulates growth, morphogenesis, and pattern formation during the development of the inner ear.

IL-10 controls cystatin C synthesis and blood concentration in response to inflammation through regulation of IFN regulatory factor 8 expression.

Cystatin C (CstC) is a cysteine protease inhibitor of major clinical importance. Low concentration of serum CstC is linked to atherosclerosis. CstC can prevent formation of amyloid β associated with Alzheimer's disease and can itself form toxic aggregates. CstC regulates NO secretion by macrophages and is a TGF-β antagonist. Finally, the serum concentration of CstC is an indicator of kidney function. Yet, little is known about the regulation of CstC expression in vivo. In this study, we demonstrate that the transcription factor IFN regulatory factor 8 (IRF-8) is critical for CstC expression in primary dendritic cells. Only those cells with IRF-8 bound to the CstC gene promoter expressed high levels of the inhibitor. Secretion of IL-10 in response to inflammatory stimuli downregulated IRF-8 expression and consequently CstC synthesis in vivo. Furthermore, the serum concentration of CstC decreased in an IL-10-dependent manner in mice treated with the TLR9 agonist CpG. CstC synthesis is therefore more tightly regulated than hitherto recognized. The mechanisms involved in this regulation might be targeted to alter CstC production, with potential therapeutic value. Our results also indicate that caution should be exerted when using the concentration of serum CstC as an indicator of kidney function in conditions in which inflammation may alter CstC production.