Intestinal regeneration as an insect resistance mechanism to entomopathogenic bacteria

Abstract

The intestinal epithelium of insects is exposed to xenobiotics and entomopathogens during the feeding developmental stages. In these conditions, an effective enterocyte turnover mechanism is highly desirable to maintain integrity of the gut epithelial wall. As in other insects, the gut of lepidopteran larvae have stem cells that are capable of proliferation, which occurs during molting and pathogenic episodes. While much is known on the regulation of gut stem cell division during molting, there is a current knowledge gap on the molecular regulation of gut healing processes after entomopathogen exposure. Relevant information on this subject is emerging from studies of the response to exposure to insecticidal proteins from the bacterium Bacillus thuringiensis (Bt) as model intoxicants. In this work we discuss currently available data on the molecular cues involved in gut stem cell proliferation, insect gut healing, and the implications of enhanced healing as a potential mechanism of resistance against Bt toxins.

Comparative Mortality and Adaptation of a Smurf Assay in Two Species of Tenebrionid Beetles Exposed to Bacillus thuringiensis

“…While chemically-induced gut leakage in our positive control is likely different from the ones induced by B. thuringiensis virulence factors, the inhibition of stem cell proliferation for gut epithelium renewal, and thus gut repair, is likely to be responsible for its leakiness during a P. entomophila oral exposure [41]. This repair mechanism is also responsible for resistance to B. thuringiensis in Lepidoptera [42], indicating that the damage caused by both these pathogens might share common mechanisms, in which case we could expect them to be both be detectable by a Smurf assay.…”

Two Phytoplasmas Elicit Different Responses in the Insect Vector Euscelidius variegatus Kirschbaum

“…On the other hand, hexamerin transcripts were upregulated upon CYp infection. Members of this protein family are effector proteins involved in insect immunity that are inducible upon ingestion of bacteria and have a putative role in gut repair (38). Moreover, in the closely related mollicute-leafhopper association (C. haematoceps/Spiroplasma citri), hexamerin is upregulated following infection and is required for vector survival after spiroplasma inoculation (36).…”

Larval Mid-Gut Responses to Sub-Lethal Dose of Cry Toxin in Lepidopteran Pest Achaea janata

“…These are the only cell present in gut capable of division and thus represent the sole source of new cells during tissue repair and growth. Continuous replacement of damaged cells by regenerative cells under toxin environment is likely to cause an alteration in cellular properties, leading to the development of resistance in insects against Cry formulations (Martinez-Ramirez et al, 1999 ; Castagnola and Jurat-Fuentes, 2016 ). Majority of cases of resistance against Cry toxins, reported reduction in binding of Bt toxins to their specific mid-gut receptors, i.e., cadherins, aminopeptidases, and alkaline phosphatases, which resulted in cross-resistance to Cry toxins sharing common altered receptor site (Morin et al, 2003 ; Pigott and Ellar, 2007 ; Zhang et al, 2009 ).…”