Display Settings:

Format

Send to:

Choose Destination
    J Mol Biol. 2004 May 21;339(1):1-15.

    Internal gene duplication in the evolution of prokaryotic transmembrane proteins.

    Source

    Department of Electronic and Information System Engineering, Faculty of Science and Technology, Hirosaki University, Hirosaki 036-8561, Japan. slsimi@si.hirosaki-u.ac.jp

    Abstract

    We investigated the evolution of transmembrane (TM) topology by detecting partial sequence repeats in TM protein sequences and analyzing them in detail. A total of 377 sequences that seem to have evolved by internal gene duplication events were found among 38,124 predicted TM protein sequences (except for single-spannings) from 87 prokaryotic genomes. Various types of internal duplication patterns were identified in these sequences. The majority of them are diploid-type (including quasi-diploid-type) duplication in which a primordial protein sequence was duplicated internally to become an extant TM protein with twice as many TM segments as the primordial one, and the remaining ones are partial duplications including triploid-type. The diploid-type repeats are recognized in many 8-tms, 10-tms and 12-tms TM protein sequences, suggesting the diploid-type duplication was a principle mechanism in the evolutionary development of these types of TM proteins. The "positive-inside" rule is satisfied in whole sequences of both 10-tms and 8-tms TM proteins and in both halves of 10-tms proteins while not necessarily in the second half of 8-tms proteins, providing fit examples of "internal divergent topology evolution" likely occurred after a diploid-type internal duplication event. From analyzing the partial duplication patterns, several evolutionary pathways were recognized for 6-tms TM proteins, i.e. from primordial 2-tms, 3-tms and 4-tms TM proteins to extant 6-tms proteins. Similarly, the duplication pattern analysis revealed plausible evolution scenarios that 7-tms TM proteins have arisen from 3-tms, 4-tms and 5-tms TM protein precursors via partial internal gene duplications.

    PMID:
    15123416
    [PubMed - indexed for MEDLINE]

      Supplemental Content

      Icon for Elsevier Science

      Save items

      loading

      Recent activity

      Your browsing activity is empty.

      Activity recording is turned off.

      Turn recording back on

      See more...
      Write to the Help Desk