2nd PU Biology 2026 | Part D All Fixed Questions with Answers | Important Questions

Hi, welcome to simplified minds. So

discuss part most important questions.

So important questions

with solutions. So, previous

model question

papers

important questions with solutions

for

important questions with solutions. So

part D section w analytics

it is [clears throat] very important

important part. So five marks questions

25 out of 25

important topics chapters

five out of five in all those chapters.

So 25 out of 25.

So our chapters

that is sexual reproduction in flowering

plants, human reproduction, principles

of inheritance, molecular basis of

inheritance, human health and disesa. So

chapters

five mark questions

with solutions.

So part 25 out of 25.

Okay. Now, so here we'll discuss about

the party fax questions of first sexual

reproduction in flowering plants. So

probable questions

explain the different outbreeding

devices developed by flowering plants or

flowering plants have developed many

devices to discourage self-pollination

and encourage crosspollination. Justify

to selfpollination discourage that is

inbreeding depression discourage

crosspollination

that is

selfcompatibility.

already it's written in handwritten

notes format.

So if [clears throat] you take the

screenshot of this particular thing.

Okay. So [clears throat] coming to

second question double fertilization

double fertilization

important concept to other questions. So

they have asked double fertilization is

a unique event taking place in flowering

plants briefly explain. So double

fertilization.

So most of the questions

okay that will fetch you some two to

three marks. Okay. Then explanation

next based on the

explanation

simple outline

primary endosperm

endpermating

antipodal cells

after this

male gamut.

So male gamut has different phase.

First,

second

that is called a singami and it is

called as triple fusion. together

primary endosperm nucleus

and together single

fusion double fertilizer

section of young an

important

connective tissue epidermis

outer single layer then middle is

helping for nourishment of the pol.

Okay. Sometimes

probability

some

fourth question part A. So this will

carry three marks. So three marks.

Some angiopermic FL sorry plants

pollinate only with the help of wind.

Why? So due to some specific adaptations

that were modified by that plant. So

adaptations.

So lack of attractive structures of the

flower

bright colors in the flower so that it

will not attract any insects or animals.

So fl usually

and it's stigma and

so production of large amount of pollen

so that high quality of lighten

lightweighten

then FL structure I explained you then

habitat usually open

so that these will be carried So example

for this is usually grass family maze

open this in this pollination occurs by

wind and trees oak pine

then next question why apple is called

false fruit which part of it forms the

fruit

false fruit difference

so true

any part will contribute to the fruit

formation. So in apple the true it's

false fruit because the phalamus is

contributing for the formation of fruit.

Right? So that's why it's called as

false fruit. So then next question read

the below given statement and answer the

given questions. A breeder is interested

in crossing different species of plants

to combine deserable characters to

produce commercially superior variety.

So what major approach in crop

improvement program would you suggest to

the breeder to achieve this goal?

uh artificial hybridization is one

technique which is very much helpful in

providing desired quality quantity or

desired quality

products.

So artificial hybridization example so

discuss in detail the techniques

involved in the process

emasculation and bagging. So

emasculation unisexual flower agitra

emasculation beta. So if it's bisexual

then it has to be emasculated and then

it has to be bagged after that it is

fused with a stigma is again bagged

after desired pollen is fertilized with

it. Okay. So process

sometimes. Okay. Okay. Then Poland

pistol interaction is a dynamic process

involving Poland recognition followed by

promotion or inhibition. Explain. So

Poland pistol interaction important

question. So Poland

pistol

recognize so that recognition is

basically chemical interaction. So two

chances there if it's compatible or if

it's the right Poland then the polen

germination happens. Followed by that

there will be postfertilization events.

If it is not compatible or if it's a

wrong poland then it rejects there will

be no germination of Poland or there is

no formation of Poland. Right? So this

is the process.

So,

so it will fetch you

terms.

Then coming to next question. Define

megasporogenesis. Describe the internal

structure of a mature embryo sack of an

angio sperm fl. So megasporogenesis

formation of mega spores from megaspo

mother cells

motherpogenesis.

So then

your egg apparatus then your antipodal

cyanogs film apparatus then your central

excel

with explanation you have to write six

of eight nuclei will be will be having

cell wall it is seven nucleated seven

Okay. So then [snorts] it is called

monosporic embryo sack, right? Okay. So

model

it's a bit application question but it

is not difficult.

So complete the given tabular column

with respect to male and female gamophy

of angioperms for the mentioned

character. Okay. So character know

number of cells present in male

gamophyte you know it's three and number

of female gamto number of cells in

mature female gamtoy seven

the number of gamuts present in male

gamophy 2 whereas in female it is one

type of cell division in development of

male gamto and female gamophy both is

meiosis you know then of the

Okay. Then which advantage offered by

seed helps angioperms adapt to changing

environmental conditions. So class I'll

discuss mi what is the advantage of

seeds for angioperms and so it has a

thick seed coat and it has sufficient

nutrients for its survival for longer

duration. So thick

longer duration nourishment even without

even in the extreme conditions till it

gets favorable conditions. So sexual

reproduction in flowering

human reproduction chapter 10 marks

sexual reproduction in flowering plants

to five marks question. So five marks

five marks 10 marks. So if you study

this 10 marks then human

reproductionally first question draw a

label diagrammatic sectional view of the

human male reproductive system and label

the given parts. So testical

glands penis epigus.

So this is all about the human

reproductive organic

epidermis and this is glands penis.

So this will give you five marks. Okay.

So important question human

reproductionally diagrammatic

representation of male and female female

then this is about diagrammatic

representation of female reproductive

system. Okay. So uterus ovary ovary

ovalop

endometrial

cervex vagina.

[clears throat]

Okay, this will give you entire marks

and then neat label diagram of sectional

view of memory gland. So

individual functions.

So so this is very very important. So

these three questions it will usually

repeat

questions or schematic representation of

spermtogenesis oris.

So spermtoenesis schematic diagram.

First miotic division, first miotic

division, secondary spermitoes.

Followed by that it will give second

miotic division spermatics which are not

active. It will further differentiate to

give spermtozoa or sperms which are

active. Okay. So this is all about

schematic representation of

spermtogenesis. Then coming to schematic

representation

or puberty

till the birth and childhood and

puberty. This will not nothing will

happen to it. After the puberty what

will happen is it will undergo the

primary oite which is which is motically

differentiated from

first miotic division first miotic

division secondary.

So this secondary

active secondary body so which will

degenerate and this is adult

reproductive life issue process.

Okay. So this is all about youris. So

you have to explain all this whatever I

told.

Okay. [clears throat]

Next obviously we studied

differenesis

and this process in the spermtoenesis

all stages of spermtoenesis will be

completed in the testice. Whereas in

major part

but the minor parts a few parts

ovalopian tub this process is continuous

whereas this is discontinuous

fetal

adult major portion complete then

followed by that. So spermatogenesis

motile sperms produce whereas youris

will produce imm

one but here many sperms millions of

sperms then cytoine

equal one sorry many active sperms

or four okay from one spermitoonium

you'll get four equal sized sperm which

is active whereas Whereas in

cytochinosis of ugonia you'll get one

large functional and non-functional

polar bodies. Okay.

So this is the difference between

spermatogenesis and genesis. So then

coming to the third chapter it is very

very important sectional section wise

analysis.

So this principles of inheritance and

variation

one is fifth mean and other is sixth. So

four questions which will carry five

marks. So it will give 20 marks.

One question which will carry five

marks. So this will give five marks. So

overall it is 20 + 5 is 25. Out of this

one question no one question no chapter.

So the total marks that you get from

this chapter is 10 marks. So please do

not leave this

part

out of 10

or

okay coming to the question. Represent

schematically the result of two gene

interaction by taking seed shape and

seed color in the plant. So seed shape

round and wrinkled. Seed color green and

yellow. Green is dominant sorry yellow

is dominant and green is recessive.

Right? So

P1 generation that is parental

generation round.

So that is dominant and this is

resistive. It will produce gamuts which

is of R Y. This is R Y. So in F1

generation you get round yellow which is

of this. So this is subjected to

selfing. Next. So you will get 9 is to 3

is to 3 is to1 phenotypic ratio. So 9 is

your round yellow. 3 is your round

green. Again the three is your wrinkled

yellow and one is your wrinkled green

which is recessive. Okay. So

ratios.

Okay. Okay. Schematically represent

incomplete dominance by taking uh

inheritance of L color in snap dragon.

So question

explain incomplete dominance with an

example. So incomplete dominance

F1 shows the phenotype

that is not present in either of the

parent.

that does not resemble either of the

parent why because

red color

in result what you're getting pink

colored fl and the genotypic and

phenotypic ratio is 1 is to2 is to1 why

this happens because factor r which is

responsible for red color is not

completely dominant over the small r

that's why it is showing incomplete

dominance so the pink color can be

distinguished from red and white. So it

is called incomplete dominance. So snap

dragon generation gamuts generation

phenotypic genotypic ratio

definition.

Okay. So this is how it is then.

So

why

so that is very simple

the F2 progeny of monohybrid cross

showed phenotypic ratio of 1 is to 2 is

to1 which is of incomplete dominance

unlike that of men's monohybrid f2 ratio

with the help of a suitable example work

out crosses and explain how it is

possible the same

incomplete dominance

P1 generation gamut

phenotypic genotypic ratio last

why because factor R is not completely

dominant over the small R

you'll get complete marks for this then

followed by that is identify the genetic

disorder so mandelian genetic disorders

important

marks Four marks

and who knows question two marks

then okay coming to the question sex

linked recessive disorder occurring in

about 8% of male and only about4% of

female leading to the defect in cone of

cells. So con cellsffectu

color blindness right. So then sex

inheritance recessive disorder affecting

a single protein involved in the

clotting of blood. Hemophilia. So

hemophilia is the disease which helps in

clotting of uh which has defect in

clotting of blood. Then the inborn error

of metabolism autotosomal recessive

trait accumulation of phenile alanine.

So the cancer phenile keonia right. So

phenile urinally phenile

then autotosomal linked recessive blood

disease substitution of amino acid in

betaglobin chain of hemoglobin it is

called as cickle cell anemia. Okay. So

keyword

then last autotosomal linked recessive

blood disease reduced rate of synthesis

of globin chains of hemoglobin. This is

actually themia. Okay. Then coming to

the next question categorize following

as either autotosomal or sex linked

disorder. So hemophilia is sex linked

disorder whereas thealismia is

autotosome linked recessive disorder

whereas phenile ketanuria is autotosomal

recessive disorder.

Okay hemophilia

it's linked disorder. Okay. What

conclusion will you arrive after careful

observation of the below diagram? So

here

so this entire hemoglobin chain

shape RBC

sole shaped RBC so it is called cle cell

anemia okay Identify the disorder by the

following symptoms individuals with

overall masculine development ment with

gynecomastia. So you know Kleinfelder

syndrome is one disorder which is

characterized by gynecomastia right so

given below is a representation of amino

acid composition of relevant translated

portion of beta chain of hemoglobin

related to shape of RBC. So question is

this representation indicates a normal

or genetically affected person? Give

reason to support your answer. Of course

this is not normal because I explained

you

so glutamic acid

in turn to sixth positional. So that's

what they have written sixth position of

beta chain has valin instead of glutamic

acid. So this is not normal. This will

give to cle cell anemic patient. Okay.

Cle cell-shaped RBC. Okay. Mention the

phenotypic difference in the normal and

affected person with respect to the

gene.

So

normal by concave shape but cle cell

anemic patient RBC shape. So this is not

normal. You don't have to write this

normal one. You have to just write this

one affected.

It is just sickle shaped RBC. Who is

likely to suffer more from the defect

related to this gene among males and

females or both equally? Why? Why? Males

and females equal

disordal

disorder related to body genes not the

sex genes. So it is both equally suffer

from this defective gene. Okay. Next

question is represent schematically the

result of one gene interaction between

pure tall pea plant and pure dwarf pea

plant. So this is all about one gene

interaction of menal. So

tall plant which has this

plant small gamut t sorry

t.

So this will give to t and t. So

you get tall

one genotypic ratio. So it will be like

this. So one will be dominant, one will

be having hetererozygous, one will be

homozygous, right?

So you have to explain this. So explain

Mendel's law of dominance with an

example and draw a conclusion. So men's

law of dominance

characters are controlled by discrete

units called factors. So factors

then factors occur in pair right

in a dissimilar pair of factors one

member of pair dominates over the other

one

and ratio. So they also asked for

conclusion. So conclusionally based on

F_sub_1 result in hetererozygous

condition T is dominant over that is

capital T is dominant over small

you'll get five marks okay so it is easy

then define unemploy give two examples

for anuploid. So

either addition or deletion of

chromosome. So usually division

additions or deletions

gain or loss of chromosome.

So two types hyperuplo and hypo hyper.

So down syndrome 21st chromosome just so

that's why it is called as 21st triomi

gain of one extra copy of 21st

chromosome it is hyperuplo and hypo

chromosome right it is an example for

autotoal this is an aloo okay fine then

write a note explanations.

Hyperuplo

that's why please listen to the class

properly. Okay. Write a note on phenile

kituria. So

[clears throat]

phenile kituria inborn error of

metabolism which is an autotosomal

recessive trait

phenile alanine

hydroxilase

enzyic. Okay. hydroxil

hydroxily

phenile phenile pyroic acid and its

derivatives.

Okay, since it is not converted to

tyrosin. Next, this will go and

aggregate to your brain and mental

retardation

pigmentation

ether disorders. So followed by that

this phenile pyrovic acid will go and

accumulate in the urine. So in urine you

can see this phenile alenin component.

So because of that it is called as

phenile ketoneura since it is found in

urine. Okay, this is all about note on

phenile phenile ketonura. So how phenile

keonora is an example for pleotrophy. So

single genome multiple phenotypic

expression.

So phenile.

So multiple phenotypic.

So

alenin hydroxilase enzyme but it will

give a lot of phenotypic things like

mental not mental retardation

pigmentation.

So it reduce the hair and skin

pigmentation which is a multiple

phenotype. So since it is giving this

disorder is showing multiple phenotypic

characters because of the single gene

mutation. It is an example for

pleotrophy. Then schematically represent

the sex determination in honeybee. So it

is very important

in this honeybee it is the case of

haplo.

So male half of what is there in the

female chromosomes. For example female

32 chromosomes. mainly it has just 16

chromosome. So if sperm and egg are

fused this is n this is hloid and this

is diploid. So you'll get female which

is of queen or work. But if male without

uh sorry if female unfertilized egg

which has two endogenesis

without fertilization if it gives to if

it gives to any this thing organism that

will lead to male. So this is what the

explanation that you have to explain. So

it is haploid sex determination right.

So okay name the genetic disorder in

which clotting of blood is affected.

Write the features of this genetic

disorder. So hemophilia I don't know XL

receive disorder where the unaffected

male car female carrier when it mates

with the male which is normal. So the

one of the female will be uh will be

carrier but the male will be affected.

Royal disorder

then

impaired clotting. So if there is any

cuts of there will be no clotting. So

immediately

mesh

clotting factors clot. Okay. So but here

there is impaired clotting where it will

lead to prolonged bleeding bleeding.

There will be unstoppable bleeding. So

because of this there will be bleeding

in muscles, joints and nose. Sometimes

this blood will also be seen in urine

and stools also. Okay. So why this

happens? Because it is exclusive primary

affecting mains. So female carrier but

male effect

clotting factor deficiency. So factor 8

is responsible and factor 9 is

responsible for deficiency of factor 8

and 9 is responsible for this. So factor

8 hemophilia a factor 9 deficient

hemophilia b

this is all about hemophilia

they have just given genetic disorder in

which clotting of blood is affected.

They have never mentioned as hemophilia.

So this is why questions will look a

little a bit longer but it is not

complex. Okay. So explain the

inheritance of blood group in human. So

blood group in human is an example for

co-ominance.

So

F1 generation both the parents resemble

chances. Okay. So here why it is called

as co-ominance. So for example blood

group

I so gene I

okay I so this gene here has I A I and

small I okay this I A and I are dominant

over the small I okay so I A small I A

express because this I A is dominant if

there is I and small I I expresses

because I is dominant if both are

present

then both will express equally that's

why it is called as co-dominance okay

that's why it is called as co-dominance

so

if the blood group is I A and small I

since it is A

blood group because it is co-dominant

with each right so this is all about

your principles of inheritance and

variation. Okay. Soap

molecular basis of inheritance. Soap

important.

So you'll

get overall 10 marks again.

Fifth

question.

Okay. DNA is genetic material in both

procarots and ukarots. Yet the packing

process in their cell is not seen.

Explain. So why proarots are called

proariots?

Proariots are called proariots because

they lack nuclear membrane. Alva. So

that is the first thing. So in procarots

there is no defined nucleus and DNA

which is of negatively charged right. So

it is negatively charged because of the

presence of phosphate group. So this

phosphate group present in the DNA is

scattered throughout the cell. So

positive charged

nucleidally.

Okay. So the DNA in nucleid is organized

in large loop held by proteins. So if

you take the example of bacterial cell

he

is a nucleid. Then coming to ukarots in

ukarots you know there is a nuclear

membrane and compartment it is more

complex but still DNA is still

negatively charged. So compensate

histone octr

positively charged protein histone is

protein. So it is positively charged

because of the presence of basic amino

acids. Basic amino acids like lysin

arginine.

So that's why it is positively charged.

So

like

beads in string format.

So it is called as chromatin chromatin

because it has eight histones but it is

a four types that's why it's called

tetrad. It's an extra information.

H2A, H2B, H2A, H2B, H3 and H4. So

basically in nucleosome you find five

types of histone that is H2A, H2B, H3

and your H1.

Okay, H2A, H2B, H3, H4 and your H1. So

five types of histone protein and it is

called octor of histones, right? So be

sting formatal. So this is all about the

nucleosome model. Then followed by that

is justify the below statements. RNA

polymerase cannot transcribe a gene by

itself. Why? Because it need helper

proteins called transcription factors

which will help in finding the promoter.

Promoter

regulation of transcription process

helper factors helper proteins that is

transcription factors. So it is not

independent.

Then transcription and translation are

separated by sight and not coupled in

ukariots. Just now we discussed in

ukarots you have compartmentalization

that is nuclear membrane. So that's why

transcription happens in your nucleus

whereas translation happens outside the

nucleus that is cytoplasm and specific

endopplasmic. Okay. So then which RNA

polymerase enzyme is involved in the

transcription of RNA? So RNA polymerase

3 is involved in the transcription of 5S

RNA and extra information it's not just

5S RNA 5S RRNA even 5S tRNA small

nuclear RNA polymerase 3 whereas your

polymer is one will help in 28 sRNA 18

SRNA 5.8 8 RNA

polymerase one. Okay. Then coming to one

very very important question or very

very important topic question.

This is uh your Griffith transforming

experiment. Okay. So

to prove that genetic material is

involved.

So transformation.

So initially they thought it is protein

but

they just conduct this experiment and

they find that there is some factor

which is responsible for transformation

of non virulent strain into vir

which is not so virulent

[clears throat]

followed by that you see a live strain

so mice dies Because

so mouse leave but heat

live

mice died. Why? Even after killing the

heat killed stain mixing it with arin

make it make this living ain virulent.

Why? What is the factor which is

transforming this R strain into

virulent?

So this is done by Frederick Griffith

actually in 1928. So explain. So this

will give you five marks followed by

that what are the functions of I gene.

So I gene it codes for represa protein.

Then lag z gene beta galactoidase lac y

gene for beta galactosides beta

galactoside permese. Then your a gene

beta galactoside transacetylase and your

inducer will be lactose. You know right

inducer lactose

which is the isomer of lactose. then

because there is very less time.

So that's why I'm going fast. Then

enumerate the characteristic of genetic

code. Genetic code is triplet in nature.

So 6ons

amino acids 22 amino acids

followed by that there is three stop

codons. Then some amino acids has more

than one codon. This is because of the

property of codon called degeneracy of

codon. Okay. Then codons are nearly

universal.

What is true for ant is also true for

elephant.

Aug methion.

Even in elephant it is coding the same

methionin. Even in us it is coding the

same methonin. Even in bacteria it is

coding the same methionin. So it is

called universal. and aug has dual

function.

Okay.

So the one function dual functionally

what is the one more function.

Okay. Then u aa u ga and u uh u a and u

mu stop code. So when this comes it is

called as termination of protein

synthesis. It is called terminator code.

Okay. So this is all about

characteristics of genetic code. Then

state the arrangement of different genes

of lactose operon. So

state the arrangement

lactose [clears throat] operon.

So here you go. lack I gene it codes for

repres

IG promoter RNA polymerase binds to this

particular uh site it will help in

transcription then operator it will help

in repressor protein that will uh block

the transcription right so then lag z

discuss the beta galactoidase beta

galactoidase help in breaking of the

lactose and uh your I will help in beta

galacto series permeas perme it will

help in uptake of the lactose into the

cell then transacetyl help in

assimilation then followed by that

structural genes which codes for protein

that's what I have written okay then

describe the role of lactose in the

regulation of lac operon so it acts as

inducer whereas it signals the cell to

produce enzymes right enzyme production

so that enzyme will in turn help in

metabolism of lactose. Then explain how

elongated DNA in ukarotic organism fits

into smallsized nucleus. So just now we

discussed how in ukarotic cell

DNA this tiny cell

DNA itself is wrapped around the

positively charged histone protein. So

DNA itself is negatively charged and it

is wrapped around the positively charged

histone protein to give nucleosome. So

histone octo

nucleosome then histone octo has eight

histone proteins.

Then it is have it is positively charged

because of abundant basic amino acids

like lysin and arginine. Followed by

that you have 200 base pairs of DNA

helith in that nucleosome. So each

nucleosome

base pairs nucleosome repeating units

chromatin fibers. So chromatin fibers.

So chromosome chroma is color and body.

So colored bodies are called as

chromosomes. Then followed by that you

know further compon

chromosomeal proteins.

So the packing of chromatin at the

higher level still

non-histone chromatin or chromosomeal

proteins help. Okay. In the context of

lac operon when jacob and monad cultured

ecoli in the presence of lactose medium

ecoli cells metabolize lactose by

synthesizing enzymes. Explain how lac

operon switch off and on. So

of lactose

in the presence of inducer that is in

the presence of lactose and absence of

lactose.

So in absence of lactose repres

I that will produce repressa protein

that will bind to your inducer. So

induced is there it is inactated.

So that is what same is explained in

diagram. So

structural gen Z Y a

individual enzymes.

So in the presence of end user

the thing is you have to write the

diagram. Okay. Then list the goals of

human genome project explanation. It's

this simple you can take the screenshot

marks five points.

Then [clears throat] describe the vatric

model of DNA with a diagram.

But still it's very simple question but

yet beautiful. So Watson 1953 based on

the data of Morris X-ray defraction data

of Morris Wilkins and Franklin Rosalen

Franklin

double helical structure of DNA

it's called double helix because it is

just twisted ladder.

So

because one runs in the direction of

five prime to three prime

to three prime

to five prime.

So it is antiparallel to each other

since it runs parall to each other based

on the two strands are paid. So I told

that bases in the strand paid

admin

cytoin hydrogen bonded. So your a will

pair with t with two hydrogen bonds and

g will pair with c with three hydrogen

bonds. And then comes charg

ratio. So it's written here. It's

important for me which will be

explained. So this is all about charg

double helical structure. So

right-handed fashion alpha helix. Okay.

So it has 10 base pair per each turn. So

major minor. So each turn is 3.4 sorry

each turn

of the helix is 3.4.

So 10

base.

It is a question for neat. Okay, you can

solve and comment if you want to. Then

explain the Hershey chain experiment to

prove that DNA as genetic matering

component

genetic material. But they did not prove

biochemically that DNA itself as genetic

material. Biochemically what root was

experiment

DNA itself as genetic material

experiment. So Alfred Hershey and Mara

Chase conducted this experiment where

they used radioactive sulfur and

radioactive phosphorus for this process.

So one the one the group of protein

bacterial fage work. So is virus

anywhere wherever you see fage it is

called virus. So bacteria affect

bacteria

virus bacteria phase

group one group of virus will be

bacterophage will be labeled with

sulfur. So sulfur you know it is present

only in protein mla and one group of

virus or bacteria phage is labeled with

your phosphorus. So phosphorus is found

in DNA.

Just now we discussed and

phosphorus.

So phosphorus rightos.

So here

DNA or genetic material.

So when they check

DNA genetic material first they infected

it is called infection second process is

blending. So they mix it well with a

media after that they centrifuge it. So

centrifuge result

first sulfur labelled

but here the phosphorus will be present

that is radioactive.

So they prove that DNA itself has

genetic matter. Okay. So then

describe the process of DNA replication

with a diagram. So you know that DNA

replication starts with or initiates

with a process in a particular spot

called origin of replication. It's

called as origin of replication or

hydrogen bond

replication unzip of DNA replication

fork form. So a hydrogen bond in a break

DNA helicase which is called as

molecular scissor right. So okay three

prime to five prime stand DNA dependent

polymer in the synthesis. So this strand

right. So here five prime to three prime

continuous

but three prime to five prime strand

continuous DNA synthesis that's why it

is called as leading strand. Here this

DNA synthesis happens in discontinuous

manner.

DNA synthesis prime to prime. So the

other way is discontinuous but the

strands which are discontinuous strands

in DNA lies

it is called as molecular stitches. So

since in the daughter DNA half of the

parent DNA and half of newly synthesized

parental strand and this is daughter

strand. So since half of the parental

strand is conserved it is called as

semicconservative method of DNA

replication. Okay. So DNA replication is

said to be semicconservative. Why?

Describe the experimental proof of

measles and install experiment um to

show DNA replication is

semicconservative. Right? So here you

go.

Measlesen install experiment. First you

have to explain why it is called as

semicconservative. Again the reason so

half of the parental strand will be

retained or conserved. That's why it's

called a semicconservative DNA

replication. So

they basically use N15 heavy isotope N15

heavy isotope

heavy isotope it's completely labeled

with the N15 by using ammonium chloride

heavy

so Eoli has the doubling time of 20

minutes so after 20 minutes

you'll have equal amount of N15 and

normal N4.

So that's why it is called as

semicconservative. Again to confirm this

after 40 minutes they again extracted

they saw the light and

heavy both equal. So that's why they

prove that cium chloride density

gradient centrifugation

it has both heavy and light isotope

that's why it is called as

semicconservative. So it confirms that

the replication of DNA is

semicconservative. Okay.

Okay.

Draw the schematic structure of a

transcription unit. This is also very

important.

promoter structural terminator. So

promotes

up.

So upstream five prime end and

of structural gene is promoter whereas

terminator is present in downstream

threep prime end of structural gene

right so it helps in binding of RNA

polymerase whereas your structural gene

it codes for the protein or polyeptide

whereas the terminator helps in ending

of the transcription unit you already

know that okay followed by at is the

difference between point mutation and

frame shift mutation. So

sorry nucleotide base

aug

ULA.

So that is an example for point

mutation. Okay. Let's see what is the

difference. So pond mutational a either

single nucleotide or single base pair

will change. Okay. So either single

nucleotide or single base.

So this help in compliment.

So this frame this frame shift

mutationally insertion or deletion of

more than one base pair

but more than one base changes. So it

results substitution insertion or it is

rare but insertion or deletion.

Okay. So here effect

it is it might be silent

missence that is single amino acid or

nonsense

but

nonfunctional or truncated protein which

is not all functional produce. This is

less lethal or less hazardous whereas

the frame shift mutation is really

hazardous. The example for this point

mutation is your cle cell anemia but

frame shift mutation or t-ac disease in

the healthy now.

Okay. Uh the last unit of your part

important is human health and disease.

So chapter five marks question.

Okay. Five marks question. So first

question differentiate innate and

acquired immunity. So you know innate

immunity is present right from the birth

and it is general non-specific and it is

first line of defense against the body.

Whereas your acquired immunity it is

also called as adaptive immunity. It is

a second line of defense. It is very

very specific. But this it is short and

immediate but it is not so effective.

Whereas your acquired immunity it is

slower than inity but it is highly

effective.

Memory sense it can be inherited. This

cannot sorry this cannot be inherited

because it is present right from the

birth. This is inherited because of the

memory cells. Okay.

Mother in the offspring. So you have to

write this. Second mention the cells

involved in accomplishing the acquired

immunity. So lymphocytes

B and Tymphosytes thymus and of fabric.

So B lymphocy then refer the below given

diagram and answer the question. Okay.

Name the molecule trapped in the lymph

nodes responsible for activation of

lymphocytes that bind to A and B site.

So

antibbody molecule

antibbody is produced by lymphocytes.

It is related to your acquired immunity.

Okay. Acquired immunity related. So the

molecule trapped in the lymph node that

is responsible for activation of

antibbody. So that is antigen. Antigen

any foreign particle that is present. It

could be you have infectious disease

causing viruses or bacteria or fungi xx

any foreign particle that is present in

the body is called as antigen. So

antigen will activate the lymphocytes to

produce antibbody. Okay. Which what does

H2 and L2 in an antibbody represent? So

it basically has two longer heavy chain.

This is heavy chain. It is longer and

smaller short chain. So

H2 heavy chain small longer so light

chain it is called as light chain.

Okay. This this is very very important.

uh the flowchart shows replication of

the retrovirus in the host. Answer the

questions given below. So here they have

written retrovirus. So retrovirus

basically it will infect the virus

normal cell. The viral RNA is introduced

in the host cell. So with the help of

reverse transcript

RNA DNA usually

DNA.

So this is viral DNA. One is viral DNA.

Then viral DNA and I viral DNA

incorporates into host genome. Right?

Then followed by that is incorporates

into host. New viral RNA is produced

by the infected cell. So this is true

right that's it. So this is very very

important flowchart

important

chances. So that's what based on that

flowchart they have asked. give an

example for retrovirus. So you know

human immuno deficiency virus is a very

famous example and human iminoirus

it is human immuno deficiency virus

deficiency

virus that is called HIV right then name

the disease caused by virus this virus

that is acquired immuno deficiencies

syndrome. So acquired name itself says

it acquired selfac

syndrome is the collection of diseases.

Because of the immuno deficiency there

will be a lot of diseases. So it is

called as acquired immuno deficiency

syndrome. Name the diagnostic test for

this disease. You know eliza that is

imino enzyme linked imosorbent assay is

the diagnostic test for this particular

disase. Okay. Name the group of genes

that have been identified in normal

cells that could lead to cancer. So you

know enco genes or protooncoins are the

genes that are responsible for your

cancer causing which techniques are used

in detecting cancer of internal organs.

So radiography there computer tomography

there methanim magnetic resonance

imaging all these techniques are used

for detecting cancer cells. Then uh why

are cancer patients often given alpha

interferons as part of treatment? So it

basically activates their immune system

and helps in destroying the tumor. So it

basically

alpha interferons

immune system activate since it is weak

and it will help in your killing of the

tumor cells that are present. Then next

question our body is provided with

different types of non-specific immunity

barriers at time of birth. So you know

what is that non-specific immunity in

immunity. So justify the above statement

with suitable example. So inate immunity

is as we discussed it is a non-specific

immunity

right from the birth immunity. So four

type of barrier produce

physical barrier physiological barrier

your cytoines and the cellular barriers.

So all these four barriers will be

present in this physical barrier

which is the first line of defense

foreign.

Then second is your mucous coating which

is present inside the internal organs

organs.

Then your physiological barriers acid

which is produced in the stomach tear

which is produced by your eyes. So it

has some enzymes which will kill the

bacteria or any particular foreign

organism. Then your saliva is also one

particular example for physiological

barrier. Then barriers bloodytes

PM and luccoytes neutrfils

monocytes natural killer cells in the

blood all these will kill the bacteria.

Then macrofasages which are present in

your blood will also cause fagocytosis

organism foreign.

So it is called fagocytosis. Then

cytoine barriers viral infected cells.

So cancer alpha interferons.

So viral infected cells will usually

secrete alpha interferons that will help

the other cells from its that will

prevent the other cells from its further

infection. Say

so be aware awake and so that's why this

interferons will be released by the

affected cell to protect the nonaffected

cell. So schematically represent the

life cycle of retrovirus in human body

with labels. Okay retrovirus for example

HIV which has RNA as its genetic

material. So it will go and attach to

the animal.

So viral protein

viral DNA reverse transcript enzyme

DNA

usually DNA

Next edna

next.

So this viral cells are ready to attack

the other cells. So this is a silent

killer retrovirus. Okay. So write the

scientific name of the organism

responsible for the cause of following

disease. So usually disease causal

causitive agent marks question.

So note typhford you know it is

salmonella ty then pneumonia is caused

by uh what is that steepus pneumonia or

pneumonia or hemophilus influenza. Then

your common cold is caused by the family

of rhino virus. Then malaria it has

plasmodium genus in the m species there

vivwax malaria m faliparam. So

falsiparam will cause the malagnant

which is the deadliest form of malaria.

Then your amibiais is caused by antimiba

histo

question. The last question of part

explain the structure of antibbody. So

just now we discussed about it. It has

it is a Y-shaped protein molecule

antibbody

imoglobulin

imoglobulin

which is written as IG. So imoglobin

it has four peptide chains as we

discussed that is two heavier longer

heavy chains and two smaller light

chains. So four chains dulfide bond in

the protein

A and B are antigen binding site.

Antigen is a foreign body I told you. So

example this is IG A, IGM, IG and IG.

Further

further.

So this is all about the structure of

antibbody. So question

most important questions with solutions.

So oi it will help you very well in your

board exam. So you are going to rock the

exam.