Behavioral Ecology and Sociobiology

, 60:815

Ovariole number—a predictor of differential reproductive success among worker subfamilies in queenless honeybee (Apis mellifera L.) colonies

  • Gustavo R. Makert
  • Robert J. Paxton
  • Klaus Hartfelder
Original Article

DOI: 10.1007/s00265-006-0225-x

Cite this article as:
Makert, G.R., Paxton, R.J. & Hartfelder, K. Behav Ecol Sociobiol (2006) 60: 815. doi:10.1007/s00265-006-0225-x


A honeybee queen normally mates with 10–20 drones, and reproductive conflicts may arise among a colony’s different worker patrilines, especially after a colony has lost its single queen and the workers commence egg laying. In this study, we employed microsatellite markers to study aspects of worker reproductive competition in two queenless Africanized honeybee colonies. First, we determined whether there was a bias among worker patrilines in their maternity of drones and, second, we asked whether this bias could be attributed to differences in the degree of ovary activation of workers. Third, we relate these behavioral and physiological factors to ontogenetic differences between workers with respect to ovariole number. Workers from each of three (colony A) and one (colony B) patrilineal genotypes represented less than 6% of the worker population, yet each produced at least 13% of the drones in a colony, and collectively they produced 73% of the drones. Workers representing these genotypes also had more developed follicles and a greater number of ovarioles per ovary. Across all workers, ovariole development and number were closely correlated. This suggests a strong effect of worker genotype on the development of the ovary already in the postembryonic stages and sets a precedent to adult fertility, so that “workers are not born equal”. We hypothesize a frequency-dependent or “rare patriline” advantage to queenless workers over the parentage of males and discuss the maintenance of genetic variance in the reproductive capacity of workers.


HoneybeePatrilineOvary developmentMicrosatelliteKin conflict

Supplementary material

265_2006_225_MOESM1_ESM.pdf (17 kb)
Supplement 1(PDF 17 kb)
265_2006_225_MOESM2_ESM.pdf (17 kb)
Supplement 2(PDF 17 kb)
265_2006_225_MOESM3_ESM.pdf (11 kb)
Supplement 3(PDF 11 kb)
265_2006_225_MOESM4_ESM.pdf (10 kb)
Supplement 4(PDF 9 kb)

Copyright information

© Springer-Verlag 2006

Authors and Affiliations

  • Gustavo R. Makert
    • 1
  • Robert J. Paxton
    • 2
  • Klaus Hartfelder
    • 3
  1. 1.Depto. Genética, Faculdade de Medicina de Ribeirão PretoUniversidade de São PauloRibeirão PretoBrazil
  2. 2.School of Biological SciencesQueen’s University BelfastBelfastUK
  3. 3.Depto. de Biologia Celular e Molecular e Bioagentes Patogênicos, Faculdade de Medicina de Ribeirão PretoUniversidade de São PauloRibeirão PretoBrazil