Gene involved in the development of segmented embryos of insects
A pair-rule gene is a type of
gene involved in the
development of the
segmentedembryos of
insects. Pair-rule genes are expressed as a result of differing concentrations of
gap gene proteins, which encode
transcription factors controlling pair-rule gene expression.[1][2] Pair-rule genes are defined by the effect of a
mutation in that gene, which causes the loss of the normal developmental pattern in alternating segments.
Pair-rule genes were first described by
Christiane Nüsslein-Volhard and
Eric Wieschaus in 1980.[3] They used a
genetic screen to identify genes required for embryonic development in the fruit fly Drosophila melanogaster. In normal unmutated Drosophila, each segment produces bristles called denticles in a band arranged on the side of the segment closer to the head (the
anterior). They found five genes – even-skipped, hairy, odd-skipped, paired and runt – where mutations caused the deletion of a particular region of every alternate segment. For example, in even-skipped, the denticle bands of alternate segments are missing, which results in an embryo having half the number of denticle bands. Later work identified more pair-rule genes in the Drosophila early embryo – fushi tarazu, odd-paired and sloppy paired.[4]
Once the pair-rule genes had been identified at the molecular level it was found that each gene is
expressed in alternate parasegments – regions in the embryo that are closely related to segments, but are slightly out of register.[5][6][7][8] Each parasegment includes the posterior part of one (future) segment, and an anterior part of the next (more posterior) segment. The bands of expression of the pair-rule genes correspond to the regions missing in the mutant. The expression of the pair-rule genes in bands is dependent both upon direct regulation by the
gap genes[9] and on regulatory interactions between the pair-rule genes themselves.[10]
^Gilbert, SF (2000).
Developmental Biology (6th ed.). Sunderland (MA): Sinauer Associates. pp. The Origins of Anterior–Posterior Polarity. Retrieved 23 October 2015.
^Wakimoto BT, Kaufman TC (January 1981). "Analysis of larval segmentation in lethal genotypes associated with the antennapedia gene complex in Drosophila melanogaster". Dev. Biol. 81 (1): 51–64.
doi:
10.1016/0012-1606(81)90347-X.
PMID6780397.
^Hafen E, Kuroiwa A, Gehring WJ (July 1984). "Spatial distribution of transcripts from the segmentation gene fushi tarazu during Drosophila embryonic development". Cell. 37 (3): 833–41.
doi:
10.1016/0092-8674(84)90418-5.
PMID6430568.
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^Macdonald PM, Ingham P, Struhl G (December 1986). "Isolation, structure, and expression of even-skipped: a second pair-rule gene of Drosophila containing a homeo box". Cell. 47 (5): 721–34.
doi:
10.1016/0092-8674(86)90515-5.
PMID2877745.
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^Lawrence PA, Johnston P, Macdonald P, Struhl G (1987). "Borders of parasegments in Drosophila embryos are delimited by the fushi tarazu and even-skipped genes". Nature. 328 (6129): 440–2.
doi:
10.1038/328440a0.
PMID2886916.
S2CID5929386.
^Howard K . & Ingham P (1986). "Regulatory interactions between the segmentation genes fushi tarazu, hairy, and engrailed in the Drosophila blastoderm". Cell. 44 (6): 949–957.
doi:
10.1016/0092-8674(86)90018-8.
PMID3955654.
S2CID28770534.