Septoria leaf blotch disease in wheat

Last updated: 24 Mar, 2015

New Phytologist Editors’ Choice April 2015

Lee, J, Orosa, B, Millyard, L, Edwards, M, Kanyuka, K, Gatehouse, A, Rudd, J, Hammond-Kosack, K, Pain, N, Sadanandom, A. 2015. Functional analysis of a Wheat Homeodomain protein, TaR1, reveals that host chromatin remodelling influences the dynamics of the switch to necrotrophic growth in the phytopathogenic fungus Zymoseptoria tritici. New Phytologist 206: 598–605

In the latest issue of New Phytologist a Rapid report by Lee et al. describes recent insights into how the fungus that causes Septoria leaf blotch disease in wheat is able to hijack the host’s signalling machinery to its own advantage. As this fungus is a major foliar pathogen and is a significant threat to yield in most wheat growing regions the work has considerable biotechnological potential.

Septoria leaf blotch disease is caused by a hemibiotrophic pathogenic fungus Zymoseptoria tritici (also known as Mycosphaerella graminicola and Septoria tritici), and it is characterised by a long, symptomless fungal growth period in host cells that is followed by a rapid switch to a necrotrophic growth phase. The necrotrophic phase results in lesions that ultimately destroy the leaves of the plant. The mechanism by which the pathogen achieves the long symptomless growth phase in the host tissue is not clear although it is known that the transition to the necrotrophic phase is associated with global reprogramming of host transcription. In their paper, Lee et al. identified a wheat homeodomain (PHD) protein, TaR1, that plays a crucial role in the transition from the symptomless to the necrotrophic growth of Septoria. The authors suggest that TaR1 contributes to this transition through its capacity to regulate gene activation at transcriptionally active chromatin.

When Lee et al. investigated TaR1 expression they found that it is maximal during the latter stage of symptom-less infection and then drops off dramatically at the transition to the necrotrophic phase. Silencing TaR1 resulted in cell death symptoms appearing earlier in infected wheat leaves, as well as reduced production of picnidia and spores by the pathogen. These observations suggest that TaR1 suppresses the defence responses of the plant and influences the ability of Septoria to reproduce asexually in wheat. The authors conclude that TaR1 helps Septoria bypass the natural defences of the plant, and this mechanism could potentially be exploited in future to develop Septoria control measures.

Fig. 2 from the paper (Lee et al.) Triticum aestivum R1 expression increases on infection. SilencingTaR1 leads to earlier onset of symptoms and reduced spore production. (a) Real-time polymerase chain reaction (RT-PCR) data shows the expression pattern ofTaR1 in both Septoria infected (grey bars) and healthy (black bars) plants over 17 d of infection. Error bars, ± standard error (SE) of the mean of raw data. (b) RT-PCR data shows the expression of TaR1 is reduced in virus-induced gene silencing (VIGS) treated plants silenced by BSMV:TaR1_A and BSMV:TaR1_B, 14 d after Barley Stripe Mosaic Virus (BSMV) treatment, compared to BSMV:00 and wild-type (Mock). Expression in the wild-type sample is set to 1 and all expression levels are given in arbitrary units relative to this. Error bars, ± SE of the mean of raw data. (c) A single leaf of BSMV:TaR1_A silenced and BSMV:00 mock silenced wheat from 10 to 18 d post-infection with Zymoseptoria tritici (left), or mock infection (right). Symptoms appear up to 2 d earlier in BSMV:TaR1_A silenced plants (day 13) compared to mock silenced (day 15), while no symptoms appear in either of the mock silenced plants. (d) Representative images showing the level of picnidia formation on mock silenced and TaR1 silenced leaves, 4 wk after infection with Z. tritici. (e) The number of picnidia produced on the leaves of TaR1 silenced plants shows about a two-fold reduction compared to mock silenced plants. Student's t-tests show a significant difference between the number of picnidia produced on the mock silenced plants and the TaR1_A (P value = 9.9 × 10⁻³) and TaR1_B (P = 5.2 × 10⁻³) silenced lines, but no difference between the two TaR1 silenced lines (P = 0.23). Error bars, ± SE of the mean of raw data. (f) Spore washes performed 4 wk after infection show a more than two-fold reduction in spores produced on TaR1 silenced plants. Student's t-tests show a significant difference between the number of spores produced in the mock silenced plants and the TaR1_A (P value = 1.4 × 10⁻³²) and TaR1_B (P = 2.4 × 10⁻³⁴) silenced lines, but no difference between the two TaR1 silenced lines (P = 0.49). Error bars, ± SE of the mean of raw data.

Alistair Hetherington, Editor-in-Chief, New Phytologist

Bristol, United Kingdom

Sarah Lennon, Managing Editor, New Phytologist

Lancaster, United Kingdom