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Mismatch Repair

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Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
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Meiosis I

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Meiosis is the division of a diploid cell into haploid cells forming sperm and eggs in animals through differentiation. Meiosis I is the first stage of meiosis, where the genetic recombination of homologous chromosomes and the reduction of the ploidy level by half occurs.
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Updated: Jun 4, 2026

Observing Mitotic Division and Dynamics in a Live Zebrafish Embryo

Observing Mitotic Division and Dynamics in a Live Zebrafish Embryo

Published on: July 15, 2016

Mutations in the pre-replication complex cause Meier-Gorlin syndrome.

Louise S Bicknell¹, Ernie M H F Bongers, Andrea Leitch

¹Medical Research Council (MRC) Human Genetics Unit (HGU), Institute of Genetics and Molecular Medicine, Western General Hospital, Edinburgh, UK.

Nature Genetics

|March 2, 2011

Summary

This summary is machine-generated.

Meier-Gorlin syndrome, a primordial dwarfism, is linked to mutations in genes controlling DNA replication. These genetic defects cause developmental abnormalities like small ears and short stature.

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Last Updated: Jun 4, 2026

Observing Mitotic Division and Dynamics in a Live Zebrafish Embryo

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Published on: July 15, 2016

Chromosome Preparation From Cultured Cells

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Published on: January 28, 2014

Area of Science:

Genetics
Developmental Biology
Molecular Biology

Background:

Meier-Gorlin syndrome is an autosomal recessive primordial dwarfism.
It is characterized by absent or hypoplastic patellae, small ears, and impaired growth.
Microcephaly is common, but intellect is typically normal.

Observation:

Individuals with Meier-Gorlin syndrome exhibit significant locus heterogeneity.
Mutations were identified in five distinct genes: ORC1, ORC4, ORC6, CDT1, and CDC6.

Findings:

All identified genes (ORC1, ORC4, ORC6, CDT1, CDC6) encode components of the pre-replication complex.
These findings implicate defects in replication licensing as the underlying cause of the syndrome.

Implications:

This research identifies specific genetic causes for Meier-Gorlin syndrome.
Understanding these defects in replication licensing sheds light on developmental abnormalities.
Opens avenues for potential future research into related growth and developmental disorders.