Gender-specific floral and physiological traits: implications for the maintenance of females in gynodioecious Lobelia siphilitica.

Journal Article (Journal Article)

A common gender dimorphism in angiosperms is gynodioecy, in which hermaphrodites and females co-occur. Females are at an inherent disadvantage because they can transmit their genes only through ovule production. One mechanism by which females can compensate for the loss of male function is by producing more seeds than hermaphrodites. As such, females should: (1) increase resource uptake to support higher seed production; and (2) allocate resources saved by the loss of male function to seed production. To test this hypothesis, we measured physiological and floral traits of gynodioecious Lobelia siphilitica, controlling for both environmental and genetic variation through a comparison of greenhouse-grown siblings. Pre-reproductive females had 14% higher area-based (Z=2.14; P=0.04) and 32% higher mass-based (Z=1.96; P=0.05) photosynthetic rate than hermaphrodites, suggesting that they have increased carbon acquisition by altering photosynthetic physiology. Female L. siphilitica produced flowers with 4-8% smaller corollas than hermaphrodites (all P<0.05), suggesting that females allocate resources away from floral structures used for pollinator attraction. The genetic correlation between genders for four floral and four physiological traits was significantly less than one but greater than zero, indicating that the evolution of gender dimorphism in response to sex-differential selection will be constrained. The allocation of resources saved by the loss of male function has been viewed as the most important mechanism allowing females of gynodioecious species to support higher seed production. Our data suggest that increased resource acquisition by females at pre-reproductive stages can also contribute to the maintenance of gender dimorphism in gynodioecious species.

Full Text

Duke Authors

Cited Authors

  • Caruso, CM; Maherali, H; Jackson, RB

Published Date

  • May 2003

Published In

Volume / Issue

  • 135 / 4

Start / End Page

  • 524 - 531

PubMed ID

  • 16228251

Electronic International Standard Serial Number (EISSN)

  • 1432-1939

International Standard Serial Number (ISSN)

  • 0029-8549

Digital Object Identifier (DOI)

  • 10.1007/s00442-003-1199-2


  • eng