The chalcone synthase multigene family of Petunia hybrida (V30): sequence homology, chromosomal localization and evolutionary aspects

1988 ◽  
Vol 10 (4) ◽  
pp. 375-385 ◽  
Author(s):  
Ronald E. Koes ◽  
Cornelis E. Spelt ◽  
Jos N. M. Mol ◽  
Anton G. M. Gerats
Gene ◽  
1989 ◽  
Vol 81 (2) ◽  
pp. 245-257 ◽  
Author(s):  
Ronald E. Koes ◽  
Cornelis E. Spelt ◽  
Peter J.M. van den Elzen ◽  
Joseph N.M. Mol

1991 ◽  
Vol 16 (4) ◽  
pp. 751-752 ◽  
Author(s):  
S. Akada ◽  
S. D. Kung ◽  
S. K. Dube

2002 ◽  
Vol 29 (12) ◽  
pp. 1500 ◽  
Author(s):  
Richard A. Jorgensen ◽  
Qiudeng Que ◽  
Carolyn A. Napoli

Transgenes designed to overexpress anthocyanin genes An6 (encoding dihydroflavonol-4-reductase) or Hf1 (encoding flavonoid-3′,5′-hydroxylase) in Petunia hybrida L. produced flower colour phenotypes similar to those caused by sense cosuppression of chalcone synthase (Chs) genes. However, unlike Chs, sense cosuppression of An6 and Hf1 resulted in female infertility in transgenotes exhibiting complete phenotypic suppression of anthocyanins. Female sterility appeared to be due to embryo abortion, with discolouration of ovules first appearing about 4 d post-fertilization, followed by gradual collapse of the ovule. Pollen from cosuppressed, female-sterile transgenotes placed on wild-type stigmas produced normal seed set, indicating that sterility of cosuppressed plants was maternally controlled. We suggest an hypothesis that cosuppression of An6 and Hf1 leads to accumulation of dihydroflavonols in the seed coat, a maternal tissue, and that this accumulation inhibits embryo growth, either directly or indirectly. In this hypothesis, direct inhibition of embryo growth would require that dihydroflavonols diffuse from the seed coat into the embryo and act there, whereas indirect inhibition would require that dihydroflavonols interfere with some capacity of the seed coat to promote embryo growth.


1986 ◽  
Vol 14 (13) ◽  
pp. 5229-5239 ◽  
Author(s):  
R.E. Koes ◽  
C.E. Spelt ◽  
H.J. Reif ◽  
P.J.M. van den Elzen ◽  
E. Veltkamp ◽  
...  

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