Thursday, 28 May 2015
Tuesday, 26 May 2015
Thursday, 21 May 2015
Repair of double-strand breaks
As we have seen, DNA complementarity is an important
resource that is exploited by many error-free correction
systems. Such error-free repair is characterized by two
stages: (1) removal of damaged and nearby DNA from one
strand of the double helix and (2) use of the other strand
as a template for the DNA synthesis needed to fill the
single-strand gap. However, what would happen if both
strands of the double helix were damaged in such a way
that complementarity could not be exploited? One way
this might happen is if both strands of the double helix
were to break at sites that were close together. A mutation
like this is called a double-strand break. If left unrepaired,
double-strand breaks can cause a variety of chromosomal
aberrations resulting in cell death or a precancerous state.
Interestingly, the ability of double-strand breaks to initiate chromosomal instability is an integral feature of some
normal cellular processes that require DNA rearrangements. One example is the generation of the diversity of
antibodies in the cells of the mammalian immune system.
Another is meiotic recombination, which uses doublestrand breaks to generate genetic diversity. As will be seen
in the remainder of this chapter, the cell uses many of the
same proteins and pathways to repair double-strand breaks
and to carryout meiotic recombination. For this reason,
we begin by focusing on the molecular mechanisms that
repair double-strand breaks before turning our attention
to the mechanism of meiotic recombination.
Double-strand breaks can arise spontaneously (for
example, in response to reactive oxygen species), or
they can be induced by ionizing radiation. Two distinct
mechanisms are used to repair these potentially lethal
lesions: nonhomologous end joining and homologous
recombination.
NONHOMOLOGOUS END-JOINING As mentioned earlier,
DNA repair is important to prevent precancerous mutations from occurring in the nondividing cells of multicellular organisms. However, when a double-strand break
occurs in cells that have stopped dividing, error-free repair
is not possible because neither of the two usual sources
of undamaged DNA is available as a template for new
DNA synthesis. That is, complementarity cannot be exploited because both strands of the DNA helix are damaged and, in the absence of replication, there is no sister
chromatid. However, as was the case for the error-prone
translesion synthesis (including the SOS system in E. coli),
the consequences of imperfect repair may be less harmful
to the cell than leaving the lesion unrepaired. In this case,
it is better to put the free ends back together so they cannot initiate chromosomal rearrangements, even if this
means that some sequence may be lost. Putting the ends
back together is accomplished by a mechanism called
nonhomologous end-joining, which involves the three steps
shown in Figure 14-32. These steps include the binding of
the broken ends by 3 proteins (KU70, KU80, and a large
DNA-dependent protein kinase) followed by the trimming of the ends so that they can be ligated together. In
mammals, several of the proteins in this pathway also
participate in the end-joining reactions associated with
the programmed rearrangements of antibody genes.
resource that is exploited by many error-free correction
systems. Such error-free repair is characterized by two
stages: (1) removal of damaged and nearby DNA from one
strand of the double helix and (2) use of the other strand
as a template for the DNA synthesis needed to fill the
single-strand gap. However, what would happen if both
strands of the double helix were damaged in such a way
that complementarity could not be exploited? One way
this might happen is if both strands of the double helix
were to break at sites that were close together. A mutation
like this is called a double-strand break. If left unrepaired,
double-strand breaks can cause a variety of chromosomal
aberrations resulting in cell death or a precancerous state.
Interestingly, the ability of double-strand breaks to initiate chromosomal instability is an integral feature of some
normal cellular processes that require DNA rearrangements. One example is the generation of the diversity of
antibodies in the cells of the mammalian immune system.
Another is meiotic recombination, which uses doublestrand breaks to generate genetic diversity. As will be seen
in the remainder of this chapter, the cell uses many of the
same proteins and pathways to repair double-strand breaks
and to carryout meiotic recombination. For this reason,
we begin by focusing on the molecular mechanisms that
repair double-strand breaks before turning our attention
to the mechanism of meiotic recombination.
Double-strand breaks can arise spontaneously (for
example, in response to reactive oxygen species), or
they can be induced by ionizing radiation. Two distinct
mechanisms are used to repair these potentially lethal
lesions: nonhomologous end joining and homologous
recombination.
NONHOMOLOGOUS END-JOINING As mentioned earlier,
DNA repair is important to prevent precancerous mutations from occurring in the nondividing cells of multicellular organisms. However, when a double-strand break
occurs in cells that have stopped dividing, error-free repair
is not possible because neither of the two usual sources
of undamaged DNA is available as a template for new
DNA synthesis. That is, complementarity cannot be exploited because both strands of the DNA helix are damaged and, in the absence of replication, there is no sister
chromatid. However, as was the case for the error-prone
translesion synthesis (including the SOS system in E. coli),
the consequences of imperfect repair may be less harmful
to the cell than leaving the lesion unrepaired. In this case,
it is better to put the free ends back together so they cannot initiate chromosomal rearrangements, even if this
means that some sequence may be lost. Putting the ends
back together is accomplished by a mechanism called
nonhomologous end-joining, which involves the three steps
shown in Figure 14-32. These steps include the binding of
the broken ends by 3 proteins (KU70, KU80, and a large
DNA-dependent protein kinase) followed by the trimming of the ends so that they can be ligated together. In
mammals, several of the proteins in this pathway also
participate in the end-joining reactions associated with
the programmed rearrangements of antibody genes.
Wednesday, 13 May 2015
NOTICE TO ALL COORDINATORS OF UBOSA BY THE PRESIDENT
ALL THE COORDINATORS OF UBOSA ARE INFORM THAT THE LATEST DAY FOR THEM TO GIVE THEIR PHOTO IS ON OR BEFORE 20/05/2015.
Saturday, 9 May 2015
SECOND SEMESTER CA TIME TABLE BY:ANDROPOV AJUATAH.A
MONDAY MLT302 9:30-11:30 U-BLOCK G
WEDNESDAY BCH302 9;30-11:30 U-BLOCK F and G
SATUDAY BCH312 7:00-9:00 RESTAU 2,3 and 4
SATUDAY BCH310 9:30-11;30 U-BLOCK G
MONDAY BCH304 9:30-11;30 AMPHI 150A,B, and C
WEDNESDAY BCH302 9;30-11:30 U-BLOCK F and G
SATUDAY BCH312 7:00-9:00 RESTAU 2,3 and 4
SATUDAY BCH310 9:30-11;30 U-BLOCK G
MONDAY BCH304 9:30-11;30 AMPHI 150A,B, and C
Friday, 8 May 2015
Thursday, 7 May 2015
major and minor grooves posted by THE PRESIDENT:ANDROPOV AJEBUA.A
The major and minor grooves are opposite each other, and each runs continuously along the entire length of the DNA molecule. They arise from the antiparallel arrangement of the two backbone strands. Note that the grooves are actual structural features of the molecule, not consequences of the way it is drawn. The grooves are important in the attachment ofDNA Binding Proteins involved in replication and trascription.
Wednesday, 6 May 2015
BCH310 TUTORIAL QUESTIONS
UNIVERSITY OF BUEA ONLINE STUDENT ASSOCIATION (UBOSA)
COORDINATOR: LOKENDO T. DEPT:
BIOCHEMISTRY AND MOLECULAR BIOLOGY
COURSE CODE: BCH 310
COURSE TITLE GENETICS
TUTORIAL SESSION
5
Date: Thursday 7th May 2015 Time: 8-11am
Motto: Thinking out of the box for
excellence
|
1) What do you understand by each of the
following?
I.
Chromosomal aberration.
II.
Synonymous mutation.
2) What is genetics? Give importance of
genetics.
3) Distinguish between the following pairs
I.
Euchromatin and heterochromatin.
II.
Constitutive and facultative heterochromatin.
4) What do you understand by the melting point
of DNA?
5)
What is
the melting point of a double stranded DNA molecule that contains
I.
27% GC?
II.
56% GC?
6) Name the major helical conformations of
DNA.
7)
What do
you understand by major and minor grooves with respect to DNA structure?
8) What are the Watson and Crick base pairs?
Why are they important?
9) Consider the following molecules: Guanine (G);
Adenine(A); Uracil(U); Thymine(T); Cytosine(C) and the following properties:
I.
Possesses at least a hydroxyl function.
II.
Possesses an amine function.
III.
Does not contain an oxygen atom.
IV.
Possesses a methyl group
V.
Can base pair wit adenine
VI.
Is a purine base.
VII.
Is a pyrimidine base.
Associate to each molecule, the number(s)
of the property(s) that is (are) applicable to it.
10) Is the intracellular messenger cAMP a
nucleoside or a nucleotide?
11) Match the following list of scientists against
their discoveries
Scientists
|
Discoveries
|
12)
Darwin and Wallace
|
I.
Genes linearly arranged on some chromosomes
and mapped.
|
13)
TH Morgan
|
II.
Related “genes” to enzymes and biochemical
processes
|
14)
Sutton Boveri
|
III.
Chromosomal theory of inheritance
|
15)
Gregor Mendel
|
IV.
Theories of acquisition of inheritable traits
|
16)
Friedrich Miescher
|
V.
Theories of evolution
|
17)
Beadle and Tatum
|
VI.
Came up with a central dogma (DNAÃ mRNAÃ Proteins)
|
18)
AH Sturtevant
|
VII.
Theories of transmission of traits
|
19)
Oswald Avery x
|
VIII.
Identified DNA in 1869
|
20)
Watson, Crick, Franklin & Wilkins
|
IX.
Genes on chromosomes
|
21)
Lamarck
|
X.
DNA was the genetic material
|
22) Give one example of each mutagens and
briefly describe how it increases the rate of mutagenesis:
II.
A DNA-modifying chemical
III.
A base analog
23) a) If the GC content of a DNA molecule is
24%, what are the percentages of the four bases (A, G, C, and T) in the
molecule?
b) What is the melting temperature of this DNA?
Good Luck
“Remember,
when you read, you skim the surface, but when you study, you discover the
treasure”
WELCOME TO THE UNIVERSITY OF BUEA ONLINE STUDY ASSOCIATION.
NOTE; IT IS ADVISABLE TO GO THROUGH QUESTION 69-82 IN THE SEMESTER EXAMINATION IN JULY 2011, THAT IS THE SECTION I OF THE PASS QUESTIONS AND ANSWERS WE HAVE. WE WILL LOOK AT THIS IN THE TUTORIAL SESSIONS.
THE ANSWERS BELOW CORRESPONDS TO ONLY Mr. BOYO'S MCQ QUESTIONS RANGING FROM 1-207.
CLICK FOR DEFINITIONS
dishomogenesis
dysplasia
immunoassay
bioassay
THE ANSWERS BELOW CORRESPONDS TO ONLY Mr. BOYO'S MCQ QUESTIONS RANGING FROM 1-207.
CLICK FOR DEFINITIONS
dishomogenesis
dysplasia
immunoassay
bioassay
UPDATED AND CORRECTED MLT302 MULTIPLE CHOICE ANSWERS
PLEASE THIS ANSWERS HAVE JUST BE UPDATED AND CORRECTED Answers for Mr.BOYO'S MCQ questions 1-206
115. C
116.A
117.E
118. B a prohormone is the inactive form of a hormone.
119. B
120.A
121. B
122. B
123. A
124.
125.A
126. A
127. B
128.B
PLEASE FOR NOW THIS IS WHAT HAVE BEEN UPLOADED......................................................................................................
STAY IN TOUCH WITH UBOSA AND MAKE THE BEST OUT OF YOUR LIFE
JESUS LOVES YOU
POSTED BY; Mr. Batenchong Simon Ebaieyong. personal adviser to the president and to the association
- C
- C
- B
- B
- D
- B
- C
- C
- D
- D
- C
- C
- E
- A
- E
- A
- B
- B
- B
- B
- B
- B
- B
- D
- A
- B
- A
- A
- B
- C
- E
- E
- D
- B
- B
- B
- B
- B reasoning; exogenous= from therapy( outside), endogenous= from within
- B
- B
Dishomogenesis is the improper pdtion and secretion of hormones - B Dysplasia is improper development of organs resulting in other effects
- A
- A
- B
- B
- B
- B
- A
- B
- D
- A
- B CBG= Corticosteriod-binding globulin
- B cortisol is a small molecule
- B
- B
- B
- B
115. C
116.A
117.E
118. B a prohormone is the inactive form of a hormone.
119. B
120.A
121. B
122. B
123. A
124.
125.A
126. A
127. B
128.B
PLEASE FOR NOW THIS IS WHAT HAVE BEEN UPLOADED......................................................................................................
STAY IN TOUCH WITH UBOSA AND MAKE THE BEST OUT OF YOUR LIFE
JESUS LOVES YOU
POSTED BY; Mr. Batenchong Simon Ebaieyong. personal adviser to the president and to the association
Monday, 4 May 2015
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