Bt Research 2025, Vol.16, No.6, 269-277 http://microbescipublisher.com/index.php/bt 271 Cry and Cyt, but to fill in the gaps - specifically targeting those bugs that Cry and Cyt cannot reach (Reyaz et al., 2019). Such a layout provides the basis for these toxins to act collectively and facilitates their "mutual borrowing" among different strains, achieving rapid expansion of the insecticidal spectrum through plasmid transfer (Guerrero et al., 2024). 3.2 Contribution of Bt plasmids to host-specific toxicity spectrum Some Bt strains specifically target Lepidoptera, while others prefer mosquitoes. This "picky eating" is often related to the combination of toxins on their plasmids. Plasmids not only determine whether there is a toxin or not, but also which toxin it is, whether it is a combination or a single approach. For instance, the H3 strain is quite typical. One of its plasmids carries 11 novel Cry proteins, showing a "preference attack" on diptera such as Aedes and Anopheles (Sun et al., 2021). Even though they are all BTS, the "Arsenal" they carry is different, and so is their coverage area. Of course, the advantages brought by these plasmids are not without cost. Their instability makes it possible for toxin genes to be lost or altered. Plasmids may also cause pathogenic fluctuations or even loss if they are out of control in terms of positioning or expression (Sheppard et al., 2016). Therefore, although plasmids are one of the key factors in the host range of Bt, they are also accompanied by variables. 3.3 Functional modules involved in the regulation and expression of Bt toxins Plasmids are not merely "storage disks" for toxin genes; some also act like "mixing consoles", controlling when and to what extent these genes are activated. pBtoxis is an example. It not only has Cry and Cyt genes, but also encodes multiple regulatory factors, and even genes related to spore formation. All these are involved in the rhythm control of toxin synthesis - synthesis when it is appropriate and suspension when it is not appropriate (Fayad et al., 2020). In addition, those inserted sequences and movable elements are not just for show; they can rearrange genes and even alter regulatory structures, enhancing the adaptability of Bt. Genes related to peptide antibiotics and secretory systems were unexpectedly found on some plasmids, which may also be involved in regulating the pathways or modalities of toxin release and affecting the "status expression" of Bt in the microbial community (Chelliah et al., 2019). The integration of these modules makes Bt not only "poisonous" but also "capable of using poison", grasping both insecticidal power and adaptability. 4 Influence of Plasmids on Bt Metabolic Pathways 4.1 Carbon source metabolism diversity and plasmid-encoded enzymes For Bt to survive in complex environments, relying solely on basic carbon source metabolism is far from enough. Some strains, such as H3, exhibit a "special ability to decompose" complex polysaccharides. This ability does not come from its chromosomes, but from the "add-ons" on the plasmid - enzymes that can break down structural carbon sources, such as chitinase and cellulase, are all encoded on its large plasmid (Fayad et al., 2020). In other words, without these plasmids, it might not even be able to consume the "food" in certain environments. This is of great significance in terms of ecological adaptability - plasmids provide an additional set of metabolic tools, allowing Bt to function smoothly in places where it "cannot be written" in the chromosomal version (Gillis et al., 2018). 4.2 Plasmid elements involved in secondary metabolite biosynthesis and regulation Bt not only needs to be able to eat and survive, but also has to have a certain deterrent effect in the microbial community. At this point, secondary metabolites come into play. And many of these substances, such as antimicrobial peptides, are backed by plasmids. For instance, the ATCC 10792 strain, with its poh1 giant plasmid, can produce "microbial killers" such as lantetin and bacitracin S, and it also carries antibiotic resistance genes, leaving itself a way out (Chelliah et al., 2019). Not only that, the germplasm plasmid regulatory module like Rap-Phr is also being adjusted - when toxins are produced and when spores are formed are no longer random but are systematic regulations linked to the external environment and the life cycle of the bacteria themselves (Figure 1) (Cardoso et al., 2020). These mechanisms give Bt an extra layer of "preparedness" when facing microbial competition or host adaptation.
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