Aging: Worms, Flies & Yeast Are More Like Us than Previously Expected

Mar 13, 2009

When it comes to the aging process, yeast, nematode worms and fruit flies have more in common with humans than previously expected. In addition to highlighting the similarities between species, a large-scale human protein network reveals a complex web of interactions among the human equivalents of the many longevity genes found in simple-animals.

The network indicates that these versions of longevity proteins are highly connected “hubs” involved in complex cellular functions. The paper also reports that the activity of encoding network proteins change during human aging. These results point to a surprisingly close relationship between aging processes in human and simpler organisms. The findings appear in the March 13, 2009 edition of the on-line, open access journal .

Buck Faculty member Robert E. Hughes, lead author of the study says that while hundreds of longevity-related genes have been identified in simple animals, there has always been a question of how relevant those genes are to humans. “This really demonstrates that there’s a strong relationship between the kinds of genes that appear to be important in human aging at the level of interaction and changes in gene expression and the kinds of genes that have been identified in large-scale in invertebrate species,” said Hughes. “This establishes a similarity in among diverse species that is perhaps a lot broader than many of us may have expected.”

The longevity was assembled from a large scale interaction map or interactions developed at Prolexys Pharmaceuticals in Salt Lake City, UT. The longevity network is comprised of 175 equivalent human versions of proteins known to influence life span in , nematode worms or flies, and 2,163 additional human proteins that interact with those proteins. Overall, the network consists of 3,271 interactions among 2,338 different proteins.

Hughes likened the connections and interactions between proteins to those commonly found in human social networking. One striking result from the network analysis was the finding that longevity proteins had an average of 19 connections as compared to an average of 14 observed for proteins in general. “These longevity proteins were unquestionably the ‘social butterflies’ of the interaction network, and therefore are likely to function as ‘hubs’ or interfaces among groups of proteins, ” said Hughes. “This really suggests that life-spans are determined by complex interactions among cellular systems and that this complexity can be observed at the level of protein interactions.” Curiously, “knocking out” the aging genes used in this study resulted in increased life span in simple organisms. Hughes says its possible that removing these highly connected “hub” genes may increase life span by preventing dysfunctional events from spreading through the cell.

A second major conclusion of the study emerged when the protein interaction network was compared with gene expression studies of done with younger and older volunteers. Statistical analysis clearly demonstrated that the network was enriched for proteins encoded by genes whose expression levels change during human aging. This surprising result further demonstrated a functional connection between human and invertebrate aging.

“This work demonstrates the value of combining high-throughput screening for protein interactions with genetic and functional validation to understand complex biological processes such as aging. Furthermore, we would like to encourage scientists interested in aging and longevity to mine the data made available in the study”, said Dr. Sudhir Sahasrabudhe, Chief Scientific Officer and the scientific founder of Prolexys Pharmaceuticals. The many proteins which have previously not been implicated in the aging process are a valuable resource for the scientific community.

The Prolexys human interactome database is by far the largest human PPI database in the world, containing over 120,000 non-redundant protein interactions and representing approximately one half of all RefSeq entries. The dataset was built using the Company’s HyNet system, a highly automated high-throughput yeast 2-hybrid process.

Source: Buck Institute for Research

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HenisDov
not rated yet Mar 16, 2009
Aging Seen Without The Emperor's New Clothes
( recapitulation )


More and more research works related to old age are published in scientific periodicals.
About time to realize that the aging of genes contributes to organisms aging.


A. Aging, lifetime and age

Aging = to become old, show the effects or the characteristics of increasing age, the increasing liferime. The effects and characteristics of not only the totality of the system, but also of each and every component, and of components of the components of the system. The system is the totality of the components.

lifetime = the duration of the existence of a living being, an organism, or an inanimate thing, a material, star or subatomic particle.

age = the length of an existence extending from its beginning to any given time.


B. More and more research works related to old age are published in scientific periodicals

The lengthening list of work-accounts comprises a wide array of subjects apparently related to old age, including:

- A variety of constitutional impairments,
- a variety of impaired biological processes,
- a variety of impaired genetic materials and expressions,
- a great variety of suggested things to consume or do or avoid for alleviating the symptoms,
- and a great variety of anti-aging suggestions.


C. Some examples of statements:

- A little stress may keep cells youthful.
- Intestinal stem cells, that replenish the lining, go awry in elderly flies, similar to what
happens in certain human stem cell populations.
- Yeast, worms and people may age by similar mechanisms.
- Nearly all organisms experience aging.
- In aging muscles and neurological problems, energy greedy organs, there are mitochondria
dysfunctions.
- Age-related growing 'leakiness' in cell nucleus membrane may contribute to aging and even to
diseases such as Parkinson's and Alzheimer's.
- Age-Related Hearing Impairment, presbycusis, is a complex elderlies disease caused by
overexpression of glutamate due to interaction between environmental and genetic factors.


D. Right they are: "Nearly all organisms experience aging". But why "nearly"?

Why don't "scientists" accept the obvious fact that genes are organisms and "experience aging", too?

Not only yeast, worms and people. Also genes and the interdependent-genes-communes, genomes. Theye are both organisms. They are alive. It is their "lifehood" that makes us and all life forms "alive".

By plain common sense - my favorite scientific approach - they should also be "experiencing aging"...


E. The aging of genes contributes to organisms aging

Since a genome is a cooperative commune of interdependent genes, many of its member genes "modulate its aging" to various extents at various time-rates depending on circumstances and environment and on their individual composition and functioning history. Various things happen to them or affect them and impair their functionalities.

In my plain commonsensical mind "interaction between environmental and genetic factors" is a description of organism's "aging". And in my boy's-like view of the emperor's new clothes organism's aging comprises aging of its genes-genome, and genes and genomes age as we age, and we age also as a result of the aging of our genes and genomes...


F. Finally, re "Theories about human cellular aging supported by new research"

http://www.eureka...1908.php

"Research presented at American Society for Cell Biology conference:
Aging yeast cells accumulate damage over time, but they do so by following a pattern laid down earlier in their life by diet as well as the genes that control metabolism and the dynamics of cell structures such as mitochondria, the power plants of cells."

Cellular Aging? What is Cellular Aging?

Complexly instrumented future spacestations accumulate damage over time, and their residents, too, age and accumulate damage over time. Yes, the functionality of the stations' residents and of their intruments and equipment is impaired with age. Wonder why?

The reason for the impairment with age of the highly active instrumented-equipped stations and of their resident crew is that they "follow a pattern laid down earlier in their life by diet as well as by the residents who control metabolism and the dynamics of the stations' structures such as mitochondria, their power plants."


G. Enough. Cells just house organisms. The resident genes-genomes are THE organisms.

About time that "scientists" refresh conceptions and comprehensions and attitudes and research plannings and peer-reviewings. Let their science evolve...


Dov Henis
(Comments From The 22nd Century)
http://blog.360.y...Q--?cq=1
Life's Manifest
http://www.the-sc...page#578
EVOLUTION Beyond Darwin 200
http://www.physfo...ic=14988&st=405&#entry396201
http://www.the-sc...age#1407

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