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Altering developmental trajectories in mice by restricted index selection

W R Atchley1, S Xu, D E Cowley

  • 1Department of Genetics, North Carolina State University, Raleigh 27695-7614, USA. atchley@ncsu.edu

Genetics
|June 1, 1997
PubMed
Summary
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Mice selected for early growth rates showed distinct changes in later development, demonstrating the genetic control over complex growth trajectories. This study explores the genetic and developmental underpinnings of growth patterns.

Area of Science:

  • Developmental biology
  • Genetics
  • Animal science

Background:

  • Understanding the genetic basis of growth is crucial for animal breeding and developmental studies.
  • Postnatal development involves complex interactions between cell proliferation (hyperplasia) and cell size increase (hypertrophy).

Purpose of the Study:

  • To investigate the genetic control of early versus late postnatal growth rates in mice.
  • To determine if selection for specific growth phases impacts other developmental stages.
  • To analyze the genetic and developmental mechanisms underlying complex growth traits.

Main Methods:

  • A restricted index selection experiment was conducted on mice over 14 generations.
  • Selection criteria focused on early (birth to 10 days) and late (28 to 56 days) growth rates.

Related Experiment Videos

  • Four distinct selection lines were established: E+LO, E-LO, EOL+, and EOL-.

    • Main Results:

    • Significant divergence in growth trajectories was observed among the selected mouse lines.
    • The observed changes in growth patterns closely matched the expected outcomes based on selection criteria.
    • Early growth rate (E) was associated with hyperplasia, while later growth rate (L) was linked to hypertrophy.

    Conclusions:

    • Selection for specific growth phases can lead to predictable changes in overall development.
    • This study highlights the genetic architecture of complex traits like growth rate.
    • The findings contribute to understanding developmental homoplasy and the genetic basis of ontogeny.