Submitted to: Journal of Plant Registrations
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 9/13/2007
Publication Date: 1/15/2008
Citation: Bregitzer, P.P., Mornhinweg, D.W., Obert, D.E., Windes, J.M. 2008. Registration of 'RWA 1758' Russian wheat aphid-resistant spring barley. Journal of Plant Registrations. 2: 5-9. Interpretive Summary: Interpretive Summary: 'RWA 1758' is a new barley cultivar that is resistant to feeding damage caused by the Russian wheat aphid. The resistance was derived by identifying a resistant "wild" barley accession held in the USDA-ARS National Small Grains Collection, and crossing this source of resistance with agronomically superior breeding lines. This is the second RWA-resistant barley cultivar to be released, and it combines good agronomic performance with a different source of resistance than in the previously-released 'Burton'. Multiple sources of resistance provide protection against variability that may be present or that may develop in aphid populations. RWA 1758 will enhance producer profitability and environmental health by enabling insecticide-free barley production in areas where RWA infestations are severe.
Technical Abstract: Technical Abstract: 'RWA 1758' (Reg. No. _______; P.I. 648913) is a spring two-rowed barley (Hordeum vulgare L.) developed by the Agricultural Research Service, U.S. Department of Agriculture. RWA 1758 was selected and released based on competitive agronomic performance and resistance to damage caused by RWA feeding. RWA 1758 derives from an BC3F3:4 selection from the cross 'Baronesse'*4/'STARS 9577B'. It was tested under the experimental designation 01ST1758. STARS 9577B is a six-rowed spring Russian wheat aphid resistant germplasm line developed and released by the USDA-ARS. STARS 9577B is resistant to the five RWA biotypes known to be present in the US. STARS 9577B was developed via selection from CIHO 4165, a landrace that was originally collected in Afghanistan. The main component of the resistance is tolerance, conferred by two dominant genes with recessive epistasis.