In this article we will discuss about:- 1. Occurrence of Albugo 2. Signs and Symptoms of the Disease Caused by Albugo 3. Mycelium 4. Fine Structure of Haustorial Apparatus 5. Economic Importance 6. Salient Features.
Contents:
- Occurrence of Albugo
- Signs and Symptoms of the Disease Caused by Albugo
- Mycelium of Albugo
- Fine Structure of Haustorial Apparatus in Albugo
- Economic Importance of Albugo
- Salient Features of Albugo
1. Occurrence of Albugo:
The genus Albugo is represented by 25 species. All are parasite on land plants. Of these A. Candida has long been known as an obligate parasite commonly found on a wide range of crucifers. Biga (1955) reported about 241 species in 63 genera are attacked by this fungal parasite.
It attacks several annual crucifers such as Capsella bursa pastoris (Fig. 6.48) Lepidium sativum, Brassica campestris, Raphanus sativus (Fig. 6.49) and several other crucifer weeds. It causes a disease called “white rust” or “blister rust”. The fungus attacks all the above ground parts.
2. Signs and Symptoms of the Disease Caused by Albugo:
The disease appears in the form of shiny, white, smooth, raised irregular blisters or patches on the leaves (Fig. 6.49) or stems (Fig. 6.48). The root is not attacked. The patches gradually turn powdery. The disease also causes deformation of flowers and fruits of the host. The distortion and hypertrophy of infected inflorescences is the most conspicuous symptom of the disease.
These distorted and hypertrophied inflorescences are called the “stag heads”. The latter contain thick-walled oospores of the parasite. Sometimes the fungus attack may cause swelling (spindle-shaped galls) and distortion of stem particularly in young plants. Infection takes place through the stomata. Extensive hypertophy, hyperplasia and chlorophyll formation accompany fungal invasion.
4. Fine Structure of Haustorial Apparatus in Albugo:
It was studied by Berlin and Powen (1964) and Coffey (1975). A dark layer of penetrating matrix known as the penetration jacket continuous with the host cell wall surrounds the haustorial stalk or neck at its proximal end.
It lies close and external to the haustorial (hyphal) wall of the neck region. External to the penetration jacket clasping the neck is a collar-like structure attached to the host cell wall and made of the same material.
The hyphal wall and plasma membrane of the intercellular haustorial mother cell are continuous along the entire length of the neck and body regions of the haustorium. These represent the haustorial wall and haustorial membrane respectively.
Berlin and Powen (1964), however, reported the hyphal wall to be absent in the distal region of the haustorial neck. It was contradicted by Coffey (1975) who found it to be intact in this region.
The protoplast of the haustorial neck has ribosomes but lacks other cell organelles. The cytoplasm of the haustorial body contains mitochondria, ribosomes and sometimes cisternae of rough endoplasmic reticulum but lacks the nuclei and perinuclear dictyosomes.
An electron dense, granular amorphous material forms the sheath matrix on the outer face of the hyphal wall of the haustorial body. The sheath matrix, also known as the extra haustorial sheath is absent in the neck region.
The invaginated host plasma membrane which completely surrounds the haustorium and remains appressed to it is called the extrahaustorial membrane. It is flexible and thrown into a series of tubular projections extending into the host cytoplasm.
Each tubule contains a dense core of material similar in appearance to and continuous with the sheath matrix. The extra haustorial or sheath membrane thus delimits the sheath or extra-haustorial matrix from the host cytoplasm and forms the interface between the two. It is obvious from the account given above that the haustorium lies outside the host cytoplasm.
It is surrounded by a thin layer of host cytoplasm covered by the tonoplast on the side facing the central vacuole of the host cell and by a sheath membrane on the side facing the haustorium.
The sheath matrix forms the physical boundary and the sheath membrane—the key to the physical relationship between the host and the obligate fungal parasite. The transport of all nutrients from the host cytoplasm occurs across the sheath membrane to the surface of the haustorium.
5. Economic Importance of Albugo:
The fungus is the causal agent of “white rust” disease of crucifers resulting in economically significant losses in the yield of turnip, rape and mustard (sarson). The distorted and hypertrophied infected inflorescences, the so-called “stage heads” consist largely of thick-walled oospores.
Another species A. ipomoeae penduraneae parasitizes sweet potato and A. bliti grows as a parasite on some members of the family Amarantaceae. As an economic disease of crucifers, white rust has a limited importance.
Heavy infection of parts above the ground may considerably reduce yield. Vanterpool (1959) estimated that white rust infecting older parts of Brassica napus may reduce yield up to 20 percent. Heavily infected flowers fail to produce seeds.
Control:
Rotation of crops, removal and destruction of infected plants from the field and spraying with fungicides such as with 0.8 percent Bordeaux mixture are the most effective methods of controlling the disease.
6. Salient Features of Albugo:
1. Albugo is an obligate parasitic fungus which attacks several species of crucifers causing the white rust.
2. The haplophase is represented by a well-developed profusely branched mycelium which consists of aseptate, conenocytic hyphae.
3.The hyphae are intercellular and feed by means of haustoria which penetrate the walls of the host cells and enlarge inside at their tips into button-like or spherical structures.
4. Asexual reproduction takes place usually by wind borne sporangia produced in chains from the tips of short, club-shaped hyphae called the sporangiophores.
5. The sporangiophores are closely packed forming a solid, palisade-like layer beneath the epidermis of the host.
6. Each sporangiophores cuts off sporangia at its tip one below the other in a long chain with the oldest at the top.
7. The pressure from below of the upwardly growing sporangiophores and the sporangia causes the host epidermis to bulge and finally to burst over the sporangial sorus.
8. The sporangial masses are exposed as a crust of white, blister-like patches.
9. The mature globose, multinucleate sporangia thus exposed -e disseminated by wind or washed by rain water to the host where they germinate to spread the disease. The factors governing germination are moisture and temperature conditions.
10. In the presence of moisture provided by rain or dew drops and at low temperature the sporangium germinates by zoospores. In dry air and at high temperature it germinates directly by a germ tube.
11. The zoospores are biflagellate, reniform, uninucleate structures. Of the two flagella one is tinsel type and other of whiplash type. They are inserted in the depression.
12. The liberals zoospore settles down on the host, withdraws its flagella, rounds off and secretes a wall around it. It then puts out a germ tube.
13. The germ tube, whether produced by the germination of zoospore or the sporangium Infects the host tissue gaining entrance through a stoma. It grows and forms the mycelium which is intercellular.
14. Sexual reproduction is oogamous and Albugo is homothallic. The antheridia and oogonia are produced near each other towards the end of the growing season.
15. Both the antheridia and oogonia are multinucleate but the functional nucleus in each is one.
16. The antheridium comes in contact with the oogonium at the side. The double wall at the point of contact dissolves. A fertilisation tube from the antheridium enters the oogonium and introduces a single male nucleus with some cytoplasm. The male and the female nuclei fuse.
17. The fertilised egg becomes an oospore by secreting a thick, warty wall around it. The oospore nucleus divides several times to produce about 32 nuclei. In this condition the oospore tides over the unfavourable period.
18. After the resting period the oospore germinates. The nuclei resume mitotic activity. The protoplast divides to form uninucleate daughter protoplast each of which becomes a biflagellate, reniform zoospore.
19. The oospore wall cracks and the zoospores pass into a thin vesicle which soon bursts open.
20. The liberated zoospores swim about in water. On coming in contact with a suitable host each settles down. The quiescent zoospore withdraws the flagella, rounds off and secretes a wall around it. Soon it puts out a germ tube which enters the host through a stoma. Within the host tissue it grows vigorously and forms the mycelium.