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#protein comparison

2 public questions tagged with this topic.

Vip proteins differ from Cry proteins because they are:

Cry proteins form parasporal crystals during sporulation, requiring solubilization at high pH and proteolytic activation. Vip proteins differ temporally and biochemically. Vip1, Vip2, Vip3 secreted during exponential vegetative growth into culture supernatant, not associated with spores. Vip3A, most agriculturally relevant, shares no sequence homology with Cry domains, presents unique tetrameric structure and binds distinct receptors including scavenger receptor class C and fibroblast growth factor receptor-like protein, triggering apoptosis pathway in addition to pore formation. Activity primarily lepidopteran but distinct from Cry1 due to different receptor usage, effective against Cry resistant strains with cadherin mutations. Stability during purification differs. Classification as vegetative insecticidal proteins emphasizes secretion stage and novelty, supporting pyramiding of Cry plus Vip to provide two modes of action in transgenic corn Viptera and cotton. Recognition of vegetative origin underpins resistance management strategy extending durability of Bt technology beyond classical crystal proteins. Transgenic stack of Cry1Ab plus Vip3Aa demonstrates 99 percent control of Helicoverpa zea even in areas with Cry resistance, validating distinct mode of action concept. Regulatory assessment includes mammalian toxicity and allergenicity studies showing Vip3 rapidly degraded in gastric fluid. Hence vegetative insecticidal proteins complement Cry library for durable resistance.

Ref: Estruch PNAS 1996 Vip vegetative; Donovan 2001 Vip3 structure; Yu Appl Environ Microbiol 1997 differences; PubMed 8855281 vegetative insecticidal proteins.

The actin cytoskeleton in prokaryotic cells is functionally similar to which of the following eukaryotic proteins?

Prokaryotic cells maintain rod shape and organize cell wall synthesis without eukaryotic compartments using cytoskeletal homologs sharing ancient ATPase fold. MreB, belonging to actin Hsp70 superfamily, shares structural core of five conserved sequence motifs forming ATP binding pocket between domains IA and IIA. Purified MreB polymerizes into ATP dependent antiparallel double filaments that rotate circumferentially beneath cytoplasmic membrane driven by cell wall elongation machinery. It scaffolds elongasome complex containing RodA glycosyltransferase, PBP2 transpeptidase and MreC MreD, directing insertion of new peptidoglycan hoops to maintain lateral wall. Depletion or inhibition by small molecule A22 causes rod to sphere transition confirming morphogenetic role, similar to actin controlling shape in eukaryotes. Keratin and vimentin are metazoan intermediate filament proteins absent in most bacteria and archaea, while ActA is Listeria monocytogenes surface protein that activates host Arp2/3 complex to form actin comet tails for motility, not bacterial cytoskeleton. Thus prokaryotic actin analog best matching functional criteria is MreB protein.

Ref: Alberts et al., Molecular Biology of the Cell, 7th ed., Chapter 16: Cytoskeleton and Bacterial Homologs MreB.