Abstract

Bract necrosis (BN) in poinsettia is thought to be caused by a localized calcium deficiency in the margins of bracts. Both calcium and silicate sprays can suppress the post-anthesis development of BN if applied repeatedly during bract development. However, studies conducted in 1993 and 1994, with BN-susceptible scions (`Supjibi') grafted onto either `Supjibi' rootstock or the BN-resistant `Annette Hegg Dark Red' (AHDR) rootstock, failed to support the calcium hypothesis. In these studies, higher calcium concentrations were found in the margins of `Supjibi' bracts on `Supjibi' rootstock, then in `Supjibi' bracts on `AHDR' rootstock, even thought the incidence of BN was highest on plants with `Supjibi' rootstock. These studies suggested that non-nutritional factors (possibly hormonal factors) may play a role in BN. In 1995, `Supjibi' plants were produced in the greenhouse, and at initial anthesis, were sprayed once with either deionized (DI) water, benzyladenine (BA) (100 ppm), or daminozide (2000 ppm). At initial anthesis, plants in all treatment groups showed a low level of BN (0.75% of bracts with symptoms). Four weeks after initial anthesis, 18.5% of bracts on DI water sprayed plants and 38.7% of bracts on daminozide treated plants had developed BN; but BA treated plants developed BN on only 1% of bracts. At final harvest (38 days after treatments were applied), BN was evident on 3.4% of BA-treated bracts, 28.7% of DI-treated bracts, and 46.3% of daminozide-sprayed bracts.

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