Correction: Genome-wide identification of the cytochrome P450 superfamily in Trichoplusia ni and in-silico expression of resistance against HDAC inhibitors

Correction to: Scientific Reports https://doi.org/10.1038/s41598-025-16919-0, published online 22 August 2025

The original version of this Article contained errors.

In the Material and method section, under the subheading ‘Transcriptomic analysis of CYP450 genes in response to HDAC inhibitors’, the original version contained wording that implied the Authors’ involvement in the generation of gene expression data, when, as also explained in the Article, the data was sourced from NCBI GEO following original deposition by Sommers et al. (Reference 35). The explanation of the experimental methods has been updated for the avoidance of doubt about the original source of the data. As a result,

“The expression data utilized in this investigation was sourced from the National Center for Biotechnology Information Gene Expression Omnibus (NCBI GEO), specifically under the accession number GSE234351 (https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE234351). Trichoplusia ni larvae were reared individually in 5 mL wells containing an artificial diet suitable for the species, supplemented with antibiotics. HDAC inhibitors (SFN or TSA) were dissolved in ethanol and applied to the surface of the diet in 30–40 µL aliquots. The ethanol was fully evaporated at 20 °C for 8 h before larval exposure. SFN was administered at concentrations ranging from 0 to 70 mM, reflecting natural levels found in cruciferous foliage. First instar larvae were introduced on Day 0 and allowed to feed ad libitum for 7 days under controlled conditions (25 °C, 50% humidity). TSA was used as a pharmaceutical control in parallel treatments at equivalent volumes³⁵. Our research endeavors to elucidate the resistance mechanisms and metabolic regulatory processes within Trichoplusia ni. To achieve this, we introduced Sulforaphane (SFN), known for its prompt alterations in enzyme activities, DNA-histone binding, and gene expression, as well as Trichostatin A (TSA), a pharmaceutical histone deacetylase (HDAC) inhibitor. Gene expression differences between control and HDAC inhibitor-treated groups (SFN and TSA) were analyzed using an unpaired two-tailed Student’s t-test. Expression values were based on normalized FPKM data, and differences were considered statistically significant at p < 0.05. The primary objective of this study is to scrutinize the impact on gene expression induced by HDAC inhibitors, namely SFN and TSA, administered through a modified artificial diet for T. ni, in comparison to the standard diet.”

now reads:

“We reanalyzed publicly available RNA-seq data from the National Center for Biotechnology Information Gene Expression Omnibus (NCBI GEO), accession number GSE234351 (https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE234351), generated by Somers et al.³⁵. Raw reads were downloaded and aligned to the T. ni reference genome, summarized to gene-level counts, and assessed for differential expression with standard normalization and multiple-testing correction. Gene expression differences between control and HDAC inhibitor-treated groups (SFN and TSA) were analyzed using an unpaired two-tailed Student’s t-test. Expression values were based on normalized FPKM data, and differences were considered statistically significant at p < 0.05. The primary objective of this study is to scrutinize the impact on gene expression induced by HDAC inhibitors, namely SFN and TSA, administered through a modified artificial diet for T. ni, in comparison to the standard diet.”

In addition, in the Results section, under the subheading ‘Expression profiling in response to SFN treatment’, one statement omitted contextually relevant citations supporting that sulforaphane (SFN) is naturally produced by plants as a defensive mechanism against insect attacks. The below References have been added and are listed as References 37–40.

37. Myzak, M. C., Karplus, P. A., Chung, F.-L. & Dashwood, R. H. A novel mechanism of chemoprotection by sulforaphane: inhibition of histone deacetylase. Cancer Res. 64, 5767–5774 (2004).

38. Ho, E., Clarke, J. D. & Dashwood, R. H. Dietary sulforaphane, a histone deacetylase inhibitor for cancer prevention. The Journal of Nutrition 139(12), 2393–2396 (2009).

39. Kaufman-Szymczyk, A., Majewski, G., Lubecka-Pietruszewska, K. & Fabianowska-Majewska, K. The role of sulforaphane in epigenetic mechanisms, including interdependence between histone modification and DNA methylation. Int. J. Mol. Sci. 16(12), 29732–29743 (2015).

40. Tortorella, S. M., Royce, S. G., Licciardi, P. V. & Karagiannis, T. C. Dietary sulforaphane in cancer chemoprevention: the role of epigenetic regulation and HDAC inhibition. Antioxid Redox Signal 22(16), 1382–1424 (2015).

Consequently,

“Sulforaphane (SFN) functions as an inhibitor of nuclear histone deacetylases (HDACs), inducing rapid alterations in enzyme activities, DNA-histone binding, and gene expression. This compound is naturally produced by plants as a defensive mechanism against insect attacks. In order to examine the impact of SFN on insect activities, transcriptomic data sourced from the NCBI GEO was analyzed to assess the significance of associated genes in response to SFN treatment. Notably, the application of SFN resulted in a significant up-regulation of the CYP4C1-1gene in T. ni (p < 0.05), as determined by Student’s t-test, indicating a pronounced biological response to SFN dosage (Fig. 7).”

now reads:

“Sulforaphane (SFN) functions as an inhibitor of nuclear histone deacetylases (HDACs), inducing rapid alterations in enzyme activities, DNA-histone binding, and gene expression. This compound is naturally produced by plants as a defensive mechanism against insect attacks^{35, 37-40}. In order to examine the impact of SFN on insect activities, transcriptomic data sourced from the NCBI GEO was analyzed to assess the significance of associated genes in response to SFN treatment. Notably, the application of SFN resulted in a significant up-regulation of the CYP4C1-1gene in T. ni (p < 0.05), as determined by Student’s t-test, indicating a pronounced biological response to SFN dosage (Figure 7).”

Finally, under the ‘Expression profiling in response to TSA treatment’ subheading, a second sentence incorrectly stated that Trichostatin A (TSA) has been used as an effective insecticide against Trichoplusia ni. The incorrect statement has been revised, and the below Reference has been added and is listed as Reference 41.

41. Bagnall, N. H., Hines, B. M., Lucke, A. J., Gupta, P. K., Reid, R. C., Fairlie, D. P. & Kotze, A. C. Insecticidal activities of histone deacetylase inhibitors against a dipteran parasite of sheep, Lucilia cuprina. Int J Parasitol Drugs Drug Resis 7(1), 51–60 (2017).

Consequently,

“Trichostatin A (TSA), a pharmaceutical histone deacetylase (HDAC) inhibitor, has been utilized as an insecticide due to its efficacy against the generalist grazer Trichoplusia ni. Transcriptomic data were utilized to analyze the expression patterns of relevant genes following TSA treatment in order to understand the effect of TSA on the cabbage looper (Fig. 8). The results demonstrate that the CYP6B5-likeand CYP4C1-2genes are significantly up-regulated in response to TSA exposure (p < 0.05), as determined by Student’s t-test. Based on the research outcomes, the identified genes were found to significantly contribute to the detoxification process of the administered therapeutic intervention in T. ni.”

now reads:

“Trichostatin A (TSA) is a pharmaceutical histone deacetylase (HDAC) inhibitor commonly used as a laboratory positive-control compound. While TSA and other HDAC inhibitors have been investigated experimentally in insects⁴¹, they are not approved or practical as agricultural insecticides. In Trichoplusia ni, TSA is largely ineffective due to strong detoxification mechanisms .Transcriptomic data were utilized to analyze the expression patterns of relevant genes following TSA treatment in order to understand the effect of TSA on the cabbage looper (Figure 8). The results demonstrate that the CYP6B5-likeand CYP4C1-2genes are significantly up-regulated in response to TSA exposure (p < 0.05), as determined by Student’s t-test. Based on the research outcomes, the identified genes were found to significantly contribute to the detoxification process of the administered therapeutic intervention in T. ni.”

As a result of the changes, the References have been renumbered.

The original Article has been corrected.